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CONCISE REVIEW |
a Laboratorio di Patologia Vascolare, Istituto Dermopatico dell’ Immacolata, Rome, Italy;
b Center for Animal Transgenesis and Germ Cell Research, Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Kennett Square, Pennsylvania, USA
Key Words. Oct-4 expression levels • Embryonic stem cell totipotency • Differentiation • Oct dimer configurations
Correspondence:
Hans R. Schöler, Ph.D., Director, Center for Animal Transgenesis and Germ Cell Research, Germline Development Group, New Bolton Center, 382 W. Street Rd., Kennett Square, Pennsylvania 19348, USA. Telephone: 610-444-5800 x2289; Fax: 610-925-8121; e-mail: scholer{at}vet.upenn.edu
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Abstract |
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 Top Abstract Oct-4: The Regulator of...What Lies Upstream?What We Know About...Epigenetic Modifications of the...The Function of Oct-4:...PORE and MORE: Two...Can There Be Mammalian...AcknowledgementsReferences |
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OCT-4: THE REGULATOR OF TOTIPOTENCY IN THE MOUSE EMBRYO |
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TopAbstractOct-4: The Regulator of...What Lies Upstream?What We Know About...Epigenetic Modifications of the...The Function of Oct-4:...PORE and MORE: Two...Can There Be Mammalian...AcknowledgementsReferences |
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The POU domain is a bipartite DNA-binding domain present in all POU proteins. It consists of two subdomains, called the POU-specific (POUS) and the POU homeo-domain (POUHD), which are connected by a flexible linker, variable in length. Flexibility of the linker region engendered between the two subdomains enables the POUS and the POUHD to contact the DNA-binding site independently of each other. Due to the particular configuration of the two POU subdomains, POU proteins have an intrinsic ability to adopt several binding configurations on the DNA. This results in an exceptional transactivation flexibility and interaction with different sets of coactivators [1]. In addition, POU factors possess an intriguing capability to form homo- and heterodimers that can bind to octamer motif variants (see below).
Mouse Oct-4 is a 352 amino acid protein belonging to class V of POU proteins. It is expressed in totipotent embryonic cells [2]. Initially expressed in all blastomeres of the developing mouse embryo, Oct-4 gene expression becomes restricted to the inner cells of the blastocyst forming the inner cell mass (ICM), and is downregulated in the trophectoderm and the primitive endoderm. Later in development, Oct-4 expression is maintained in the embryonic ectoderm at the egg-cylinder stage and is downregulated at gastrulation in an anterior-posterior pattern. The only cells maintaining Oct-4 expression after this stage are primordial germ cells (PGCs) arising within the extraembryonic mesoderm at 7.2 days of mouse embryo development. Germ cells maintain the expression of Oct-4 until the initiation of sexual differentiation of the gametes and meiosis, in the female at day 13-14 post-coitum (dpc) and at the beginning of spermatogenesis in the newborn males [3].
Oct-4 ortholog genes share a high degree of genomic structural organization and sequence conservation and have been identified in other mammalian species including human, bovine, and rat [3]. Sequence comparison of the promoter/ enhancer regions of the mammalian Oct-4 genes with that of the mouse ortholog revealed a common organization of cis-regulatory elements that are supposed to function in a similar fashion during embryonic development [4]. The analysis of the endogenous Oct-4 protein expression shows that in bovine and porcine preimplantation embryos, Oct-4 is not restricted to totipotent cells [5, 6]. In addition, it was found that the expression of green fluorescent protein controlled by the promoter/enhancer regions of the murine Oct-4 gene microinjected into fertilized bovine and porcine oocytes, was not restricted to cells of the ICM [6]. In contrast, the expression of human Oct-4 is comparable to the pattern in the mouse, suggesting that it may have a similar function in preventing human totipotent embryo cells from differentiating [7].
The unique Oct-4 expression pattern in the mouse embryo has led to the hypothesis of the "totipotent cycle" [8]. According to this postulate, cells losing Oct-4 during embryonic development differentiate into somatic lineages whereas cells maintaining Oct-4 expression retain totipotency and have the competence to develop into germ cells.
Oct-4 function has recently been abolished by homologous recombination [9]. Oct-4–/– embryos die at the time of implantation due to a failure to form the ICM. In vitro culture of Oct-4–/– embryos revealed that the loss of Oct-4 changes the fate of cells destined to become ICM cells to differentiate to a trophectoderm lineage. Interestingly, suppression of Oct-4 function does not influence the maintenance of the totipotent phenotype of the blastomeres prior to the formation of the blastocyst. This suggests that Oct-4-dependent transactivation in the early mouse embryo begins to be essential for maintaining a totipotent cell phenotype when the first somatic lineage (the trophectoderm) splits from the totipotent compartment (the ICM). Thus, the decision to maintain Oct-4 in the inner cells of the compacted morula and downregulate it in the outer cells appears to be one of the crucial events that enables the proper development of the preimplantation embryo [10] (Fig. 1
).
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Oct-4 has recently been purported to have an even more important function in early mouse embryonic development. It was shown that it is not only involved in the maintenance of totipotency and self-renewal of the stem cell population of the preimplantation embryo, but it may also play a role in the initiation of the pathways controlling the early differentiation of the primitive endoderm from totipotent ICM cells (Fig. 1
).
In a study examining Oct-4 protein expression at early stages of mouse development, it was reported that Oct-4 is transiently increased in the primitive endodermal cells (EC) of the blastocyst, prior to final downregulation [11]. The function of Oct-4 transient upregulation in primitive EC was suggested from the evidence that Oct-4 is implicated in the regulation of the Osteopontin gene (OPN), encoding an extracellular matrix component involved in cellular migration. Botquin et al. [12] found that retinoic acid treatment of F9 EC cells, that are usually used as a model for differentiation of the primitive endoderm, results in a transient increase of Oct-4, paralleled by an increased expression of OPN. A search for Oct-4 potential binding sites within the cis-regulatory sequences of the OPN gene identified a novel palindromic sequence named palindromic-oct-regulatory-element (PORE) within the first intron of OPN. This sequence contains a consensus octamer motif and an inverted half-site CAAAT spaced by two nucleotides to which Oct-4 binds in vivo as a monomer and a homodimer [12]. A comparison of the transcriptional activities of the mono- and dimeric configurations was performed by transient transfections of reporter vectors bearing mutated OPN Oct-4-binding sites of which one binding configuration was abolished leaving the other unaffected. This analysis revealed that the Oct-4 dimer plays a major role in OPN enhancer activity whereas the monomer has only weak effects [12]. This in turn suggests that the canonical octamer motif is not sufficient, per se, to create a strong Oct-4 activation site unless it is enclosed in a sequence context allowing Oct-4 to crosstalk with appropriate coactivators or form dimers (see below).
Recently, a strategy using inducible Oct-4 expression coupled to homologous recombination of the endogenous Oct-4 gene was applied to demonstrate dose-dependent phenotypic effects of Oct-4 in embryonic stem (ES) cells. Niwa et al. [13] introduced a tetracycline-tTA Oct-4 transgene into ES cells in which one copy of the endogenous Oct-4 gene was knocked-out [14]. Transfection of the cells in the absence of tetracycline (Tc) caused up to a twofold increase in Oct-4 expression relative to endogenous levels. Under these conditions, ES cells differentiated and formed clones of primitive endoderm cells as shown by upregulation of the GATA-4 gene [15]. A targeting of the second endogenous copy of Oct-4 was then performed in the same cells. Thus, ES cells were obtained which expressed a sufficient level of Oct-4 to maintain totipotency due to the introduced transgene. In addition, the possibility of repressing the expression of the transgene by treating the cells with different amounts of Tc provided a precise evaluation of the minimal Oct-4 level required for the maintenance of stem cell totipotency. As in the case of Oct-4–/– embryos [9], loss of Oct-4 caused ES cells to differentiate into trophectoderm. Interestingly, this only occurred when less than 50% of the normal expression level of Oct-4 was achieved by treating the cells with increasing amounts of Tc. Altogether, these results suggest that either an increase above 150% or a decrease below 50% of the endogenous Oct-4 levels can serve as a trigger for the differentiation of the two somatic lineages in mouse preimplantation embryos [16] (Fig. 1).
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WHAT LIES UPSTREAM? |
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TopAbstractOct-4: The Regulator of...What Lies Upstream?What We Know About...Epigenetic Modifications of the...The Function of Oct-4:...PORE and MORE: Two...Can There Be Mammalian...AcknowledgementsReferences |
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A unique cellular identity of the blastomeres is maintained until compaction of the morula. At this stage, an inner compartment of cells is segregated from the outer layer of cells that will form the trophectoderm. It has been found that a differential gene expression pattern in the outer cells of the compacted morula is established prior to the differentiation of these cells into trophectoderm [17]. One possibility is that this gradient may be due to the different polarity and cell contacts established between outer and inner cells of the compacted morula. Therefore, genes like Oct-4 that are initially equally expressed in all cells of the embryo may be repressed as a consequence of specific cell-cell adhesion, thereby allowing the upregulation of genes involved in the formation of the trophectoderm.
Another possible explanation as to the differences in Oct-4 expression between inner and outer cells of the preimplantation embryo suggests that repressors that are unequally distributed in the oocytes may be differentially inherited by inner and outer blastomeres during cleavage. However, the only report showing that a similar mechanism may act in the mouse was the observation that a gradient of the leptin/STAT-3 proteins is formed in the mouse oocyte and may be conserved throughout the early cleavage stages [18]. This makes it unlikely that differential expression of Oct-4 in the compacted morula may be regulated by an unequal distribution of determinants laid down in the oocyte.
Recent observations have suggested that the main symmetry of the mouse embryo could be laid down long before the morphological appearance of the antero-posterior axis at gastrulation. It has been shown that the position of the second polar body that is formed after fertilization and remains associated to the embryo up to the blastocyst stage correlates with the prospective bilateral symmetry axis of the mouse embryo [19]. An asymmetrical distribution or proliferation of cells forming the nascent visceral endoderm (VE) between the region of the ICM close to the polar body and the region away from it is established as early as day 5.5 dpc [20]. Interestingly, VE cells arising from cells of the ICM close to the polar body cover the embryonic ectoderm and migrate from the prospective posterior pole towards the anterior whereas VE cells originating from distal ICM cells mainly cover the extraembryonic ectoderm [20]. VE cells covering the epiblast and migrating towards the anterior have been found to express a number of genes that are supposed to play a role in the establishment of the A-P axis prior to the beginning of gastrulation [21]. Therefore, the finding that the VE is formed according to an A-P fashion prior to 5.5 dpc suggests that the overall A-P structure of the embryo could be established during preimplantation development.
How does Oct-4 fit into this process? Up to now there is no evidence supporting the notion that Oct-4 could be differentially expressed in individual cells of the ICM. However, the transient upregulation of Oct-4 protein [11] that is now correlated to OPN overexpression [12] and initiation of the genetic program of the primitive endoderm differentiation [13, 16] strongly suggest that this may be the case. Since in situ hybridization studies have failed to detect differences in Oct-4 mRNA levels in the ICM [11], it is likely that post-translational mechanisms and/or an increased stability of the Oct-4 protein may be involved in Oct-4 regulation.
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WHAT WE KNOW ABOUT OCT-4 REGULATION |
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TopAbstractOct-4: The Regulator of...What Lies Upstream?What We Know About...Epigenetic Modifications of the...The Function of Oct-4:...PORE and MORE: Two...Can There Be Mammalian...AcknowledgementsReferences |
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Transgenic mice and studies in ES cell lines have addressed Oct-4 regulation in stem cells and in developing mouse embryos. Analysis of transgenic mice carrying the LacZ reporter under the control of an 18 kb fragment from the Oct-4 genomic sequence allowed the identification of elements that play important roles in Oct-4 gene expression [22]. Two elements named proximal enhancer (PE) and distal enhancer (DE), based on their position with respect to the transcription initiation site, regulate the stem cell-specific activity of Oct-4. Mice carrying the Oct-4 transgene lacking a 1-kb fragment containing the PE did not express LacZ in the epiblast whereas deletion of a 3.2-kb fragment including the DE caused abolition of LacZ activity in the ICM and germ cells [22]. The differential in vivo activity of the Oct-4 enhancers is recapitulated in ES cells and EC that resemble cells of the ICM and the epiblast, respectively. The DE is active in ES cells whereas the PE is active in EC. An in vivo footprinting study has allowed the identification of the precise binding sites within the two enhancers that are bound by transcription factors [23]. One site named 1A was found to be located within the PE and another site named 2A was identified in the DE [23]. Strikingly, these sites exhibit nearly identical sequence homology to the GC-box, and are both protected in undifferentiated ES and EC cells, and released from such protection upon retinoic acid differentiation of either cell type [23]. Electrophoretic mobility shift assays have shown that both ES and EC cells express proteins that are able to bind these sites in an identical fashion [K. Hübner and H.R.S., unpublished]. Thus, although sites 1A and 2A are crucial for the activity of the PE and the DE, the occupancy data do not support their involvement in the stem cell-specific activities of the two enhancers in vivo. This suggests that other unknown cis-acting elements within the DE and PE act in concert with sites 1A and 2A in determining the specific activity of the two enhancers in different stem cell lines and during embryogenesis.
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EPIGENETIC MODIFICATIONS OF THE CHROMATIN STRUCTURE MAY PLAY A ROLE IN OCT-4 EXPRESSION AND DOWNREGULATION DURING EMBRYONIC DEVELOPMENT |
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Oct-4 gene expression is potentially affected by methylation although it is not subject to imprinting. Ben-Shushan et al. reported that Oct-4 gene activity extinction in stem cell x fibroblast hybrid cells is accompanied by a rapid methylation of CpG islands in the promoter and the PE [25]. Methylation of regulatory sequences such as the PE and the DE may play a role in Oct-4 shutdown occurring during gastrulation, when a wave of de novo methylation is reported to occur in the somatic cells of the embryo [26]. Segregation of PGCs into an extraembryonic tissue such as the extraembryonic mesoderm may prevent methylation of their genome and germ cell differentiation [8]. Again, this suggests that maintenance of Oct-4 expression in PGCs, and therein of mammalian germline totipotency, may be a consequence of germ cells escaping from general epigenetic reprogramming of the chromatin that occurs in epiblast cells at the time of gastrulation.
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THE FUNCTION OF OCT-4: ACTIVATION/SUPPRESSION OF TRANSCRIPTION, DIMERIZATION POTENTIAL, AND FUNCTIONAL PARTNERS |
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TopAbstractOct-4: The Regulator of...What Lies Upstream?What We Know About...Epigenetic Modifications of the...The Function of Oct-4:...PORE and MORE: Two...Can There Be Mammalian...AcknowledgementsReferences |
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Oct-4 was reported to act as a repressor of specific target genes in two cases. Octamer motifs located within the proximal promoters of the 
and ß subunit of the human chorionic gonadotropin (hCG) genes mediate Oct-4 transrepression of both genes in choriocarcinoma cells [29, 30]. Alleviation of hCG gene repression due to Oct-4 downregulation in the outer cells of the compacted morula may be one of the initial events which establish a gene expression pattern leading to the trophectoderm lineage.
Repression is by no means the most effective or the only way of Oct-4 target gene regulation in stem cells. Oct-4-dependent transcriptional transactivation from either proximally or remotely located binding sites in totipotent cells has been reported. Distance-dependent Oct-4 transactivation is a unique property of embryonic cells that is mediated by specific sets of coactivators connecting a remotely bound Oct-4 molecule to the transcriptional machinery.
The adenoviral E1A protein was the first protein found to functionally interact with Oct-4 [31]. In differentiated cells, E1A substitutes for the stem cell-specific bridging factor(s) enabling distance-dependent transactivation. An interaction between the Oct-4 POU domain and the zinc-finger motif contained within the constant region 3 (CR3) of E1A is responsible for this functional cooperation [31]. In addition, we have recently found that regions other than CR3 contribute to the interaction between Oct-4 and E1A [32, 33]. E1A and E1A-like proteins in stem cells mediate Oct-4 distance transactivation by bridging Oct-4 molecules to the basal transcription machinery. It has been suggested that this activity does not require binding of this coactivator to DNA [31] (Fig. 2).
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An Oct-4/Sox-2 complex positively regulates the expression of another stem cell-specific gene. Utf1 is a transcriptional activator expressed specifically in the ICM of the mouse embryo [39]. Like FGF-4, Utf1 is regulated by an enhancer element localized in the 3'-UTR to which Sox-2 and Oct-4 bind and form a complex [40]. Cooperative fixation of both Sox-2 and Oct-4 to their adjacent binding sites is necessary for the activity of the Utf1 enhancer, again demonstrating that none of the two transcription factors is able to transactivate on their own [40] (Fig. 2).
Sox-2 represents an important sequence-dependent Oct-4+ coregulator but it can also negatively regulate Oct-4 activity. The formation of the Oct-4 dimer on the PORE (see above), can be counteracted by Sox-2-binding onto one of the half sites of the PORE, thus resulting in the formation of an Oct-4/Sox-2 complex [V. Botquin and H.R.S., unpublished observations]). Accordingly, cotransfection of Oct-4 expression vectors with increasing amounts of Sox-2 expression vector does repress the activity of the Oct-4 dimer in 293 cells [12]. Since Sox-2 is reported to be downregulated in stem cells prior to Oct-4 shutdown [12], it is possible that relief of Sox-2 interference resulting in Oct-4 dimer formation may cause the transient OPN overexpression that marks the lineage of the primitive endoderm. Thus, it appears that in addition to increased Oct-4 protein levels, as suggested by the experiments performed by Niwa et al. [13], a differential stoichiometry of the interaction of Oct-4 with functional partners could also regulate Oct-4 transactivation in totipotent cells (see below).
HMG proteins have been reported to interact and functionally cooperate with POU proteins in a binding site-independent fashion [4]. Using the novel approach of phage display, we have recently identified HMG-1 and HMG-2 as two factors that are able to interact with Oct-4 in coimmunoprecipitation assays. Transfection of HMG-1 into EC cells causes an increase in Oct-4 transactivation of reporter vectors bearing six copies of the consensus octamer motif cloned at a distance from a minimal TK promoter (6W enhancer) [31], thus providing the first example of a nonviral factor that contributes to Oct-4 activity in stem cells [33]. Although it is not likely that HMG-1 represents a coactivator like E1A, which connects Oct-4 with the basal transcription machinery, it is possible that the interaction between HMG-1 and Oct-4 contributes to the stabilization of the Oct-4/DNA complex and/or to the activation of Oct-4 transactivation domains.
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PORE AND MORE: TWO ALTERNATIVE OCT-DIMER CONFIGURATIONS REFLECTING THE FUNCTIONAL PLASTICITY OF POU PROTEINS |
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TopAbstractOct-4: The Regulator of...What Lies Upstream?What We Know About...Epigenetic Modifications of the...The Function of Oct-4:...PORE and MORE: Two...Can There Be Mammalian...AcknowledgementsReferences |
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). The MORE sequence has been obtained by inserting the POUS ATGC subsite within the Pit-1 dimer-binding sequence [41]. MORE mediates the formation of homo- and heterodimers of virtually all mouse Oct factors [42]. The important difference between the PORE and the MORE dimer configurations revolves around the arrangement of the POUS and POUHD. In the case of the PORE, the two subdomains of the same Oct molecule occupy one half-site whereas in case of the MORE, the POUS and POUHD domains of two different Oct molecules make contacts with each half-site. Strikingly, in the presence of the coactivator OBF-1 (OCA-B, BOB-1) [43], Oct-1 activates transcription only when it is bound to the PORE whereas it is not active on the MORE. Indeed, the crystal structure of the Oct-1/MORE dimer revealed that the binding configuration of Oct-1 to the MORE locks the docking site of OBF-1 on the Oct-1 protein, thus impairing interaction and functional cooperation [42]. It is possible that other coactivators may be differentially associated with different POU protein dimer configurations based on the particular arrangement of the DNA binding site. The MORE and PORE provide two alternative ways of forming POU protein dimers resulting in differential availability of interfaces for the interaction with associated factors. This issue opens the possibility of another level of complexity of transcriptional regulation by POU proteins.
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CAN THERE BE MAMMALIAN LIFE WITHOUT POU PROTEINS? |
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TopAbstractOct-4: The Regulator of...What Lies Upstream?What We Know About...Epigenetic Modifications of the...The Function of Oct-4:...PORE and MORE: Two...Can There Be Mammalian...AcknowledgementsReferences |
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The differentiation of ES cells to trophoblast cells in which Oct-4 expression levels are reduced can be explained in terms of a simple model of transactivation involving the crosstalk with a bridging factor like E1A or a cofactor such as Sox-2. This model implies that a reduction of Oct-4 protein expression causes a reduction of the activity of Oct-4 target genes (such as FGF-4) [10], or the de-repression of other target genes (such as and ß hCGs, see above) due to a limiting amount of Oct-4. However, the same model cannot account for the primitive endoderm phenotype that results from an increase in Oct-4 expression level in ES cells. In fact, it has been shown that Oct-4 overexpression causes a reduction of 6W enhancer transactivation due to squelching of E1A [31]. Therefore, an increase in Oct-4 expression levels should be linked to a reduction of the ability of Oct-4 to activate target genes and result, in principle, in a similar phenotype of the cells in which Oct-4 protein is downregulated. One possible explanation as to why this is not the case is that an increase in Oct-4 protein levels may modify the balance between Oct-4/Oct-4 homodimers and Oct-4/Oct-6 and/or Oct-4/Oct-1 heterodimers. This may result in a change of the overall dimeric Oct-dependent transactivation in stem cells. Similar to the explanation offered for the increase in PORE activity in primitive EC [12] (see above), the activity of Oct-4 target genes may be increased by forcing the formation of Oct-4 homodimers.
To date, the existence of a transcriptional "equilibrium" established by the maintenance of precise levels of dimers containing Oct-4 and other Oct proteins driving the activity of genes involved in the self-renewal of ES cells is only a matter of speculation. However, the possibility of artificially modifying Oct-4 expression levels using inducible expression systems has now provided the first evidence that the perturbation of this equilibrium can result in specific phenotypic changes of stem cells. This has definitely led to new ways of looking at the differentiation of totipotent cells as a process that is dynamically driven by the relative expression levels of a unique transcription factor, prior to the establishment of a specific gene expression pattern.
Given the striking feature of POU proteins to adopt several binding configurations involving differential interaction with coactivators, it can be predicted that modifications of the relative levels of other Oct factors that are known to be expressed in a tissue-specific manner during mouse embryogenesis [45] may play a major role in the initial events of tissue modeling during embryogenesis. Experiments using systems to control up- and downregulation of the Oct proteins in vivo are therefore necessary to determine whether, as in the case of Oct-4, modifications of their relative levels determine a major "reprogramming" of the cell fate during mouse development.
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Acknowledgements |
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TopAbstractOct-4: The Regulator of...What Lies Upstream?What We Know About...Epigenetic Modifications of the...The Function of Oct-4:...PORE and MORE: Two...Can There Be Mammalian...AcknowledgementsReferences |
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REFERENCES |
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 Z.-X. Wang, C. H.-L. Teh, J. L. L. Kueh, T. Lufkin, P. Robson, and L. W. Stanton Oct4 and Sox2 Directly Regulate Expression of Another Pluripotency Transcription Factor, Zfp206, in Embryonic Stem Cells J. Biol. Chem., April 27, 2007; 282(17): 12822 - 12830. [Abstract] [Full Text] [PDF]
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J. Jones and T. A. Libermann Genomics of Renal Cell Cancer: The Biology Behind and the Therapy Ahead Clin. Cancer Res., January 15, 2007; 13(2): 685s - 692s. [Abstract] [Full Text] [PDF]
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M. Kanatsu-Shinohara, K. Inoue, N. Ogonuki, H. Miki, S. Yoshida, S. Toyokuni, J. Lee, A. Ogura, and T. Shinohara Leukemia Inhibitory Factor Enhances Formation of Germ Cell Colonies in Neonatal Mouse Testis Culture Biol Reprod, January 1, 2007; 76(1): 55 - 62. [Abstract] [Full Text] [PDF]
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J. A. Byrne, S. M. Mitalipov, L. Clepper, and D. P. Wolf Transcriptional Profiling of Rhesus Monkey Embryonic Stem Cells Biol Reprod, December 1, 2006; 75(6): 908 - 915. [Abstract] [Full Text] [PDF]
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L. Zeng, E. Rahrmann, Q. Hu, T. Lund, L. Sandquist, M. Felten, T. D. O'Brien, J. Zhang, and C. Verfaillie Multipotent Adult Progenitor Cells from Swine Bone Marrow Stem Cells, November 1, 2006; 24(11): 2355 - 2366. [Abstract] [Full Text] [PDF]
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 C. Sagrinati, G. S. Netti, B. Mazzinghi, E. Lazzeri, F. Liotta, F. Frosali, E. Ronconi, C. Meini, M. Gacci, R. Squecco, et al. Isolation and Characterization of Multipotent Progenitor Cells from the Bowman's Capsule of Adult Human Kidneys J. Am. Soc. Nephrol., September 1, 2006; 17(9): 2443 - 2456. [Abstract] [Full Text] [PDF]
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 R. J. B. Francis and C. W. Lo Primordial germ cell deficiency in the connexin 43 knockout mouse arises from apoptosis associated with abnormal p53 activation Development, September 1, 2006; 133(17): 3451 - 3460. [Abstract] [Full Text] [PDF]
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 R. P. Redvers, A. Li, and P. Kaur Side population in adult murine epidermis exhibits phenotypic and functional characteristics of keratinocyte stem cells PNAS, August 29, 2006; 103(35): 13168 - 13173. [Abstract] [Full Text] [PDF]
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G. Pan, J. Li, Y. Zhou, H. Zheng, and D. Pei A negative feedback loop of transcription factors that controls stem cell pluripotency and self-renewal FASEB J, August 1, 2006; 20(10): 1730 - 1732. [Abstract] [Full Text] [PDF]
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S Tielens, B Verhasselt, J Liu, M Dhont, J Van Der Elst, and M Cornelissen Generation of embryonic stem cell lines from mouse blastocysts developed in vivo and in vitro: relation to Oct-4 expression Reproduction, July 1, 2006; 132(1): 59 - 66. [Abstract] [Full Text] [PDF]
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 H. Yu, D. Fang, S. M. Kumar, L. Li, T. K. Nguyen, G. Acs, M. Herlyn, and X. Xu Isolation of a Novel Population of Multipotent Adult Stem Cells from Human Hair Follicles Am. J. Pathol., June 1, 2006; 168(6): 1879 - 1888. [Abstract] [Full Text] [PDF]
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S. R. Hough, I. Clements, P. J. Welch, and K. A. Wiederholt Differentiation of Mouse Embryonic Stem Cells after RNA Interference-Mediated Silencing of OCT4 and Nanog Stem Cells, June 1, 2006; 24(6): 1467 - 1475. [Abstract] [Full Text] [PDF]
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K. Nganvongpanit, H. Muller, F. Rings, M. Hoelker, D. Jennen, E. Tholen, V. Havlicek, U. Besenfelder, K. Schellander, and D. Tesfaye Selective degradation of maternal and embryonic transcripts in in vitro produced bovine oocytes and embryos using sequence specific double-stranded RNA. Reproduction, May 1, 2006; 131(5): 861 - 874. [Abstract] [Full Text] [PDF]
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 H. J. Han, J. S. Heo, and Y. J. Lee Estradiol-17beta stimulates proliferation of mouse embryonic stem cells: involvement of MAPKs and CDKs as well as protooncogenes Am J Physiol Cell Physiol, April 1, 2006; 290(4): C1067 - C1075. [Abstract] [Full Text] [PDF]
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M. Kanatsu-Shinohara, K. Inoue, J. Lee, H. Miki, N. Ogonuki, S. Toyokuni, A. Ogura, and T. Shinohara Anchorage-Independent Growth of Mouse Male Germline Stem Cells In Vitro Biol Reprod, March 1, 2006; 74(3): 522 - 529. [Abstract] [Full Text] [PDF]
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 C. Matthai, R. Horvat, M. Noe, F. Nagele, A. Radjabi, M. van Trotsenburg, J. Huber, and A. Kolbus Oct-4 expression in human endometrium Mol. Hum. Reprod., January 1, 2006; 12(1): 7 - 10. [Abstract] [Full Text] [PDF]
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J. S. Heo, Y. J. Lee, and H. J. Han EGF stimulates proliferation of mouse embryonic stem cells: involvement of Ca2+ influx and p44/42 MAPKs Am J Physiol Cell Physiol, January 1, 2006; 290(1): C123 - C133. [Abstract] [Full Text] [PDF]
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A. Buageaw, M. Sukhwani, A. Ben-Yehudah, J. Ehmcke, V. Y. Rawe, C. Pholpramool, K. E. Orwig, and S. Schlatt GDNF Family Receptor alpha1 Phenotype of Spermatogonial Stem Cells in Immature Mouse Testes Biol Reprod, November 1, 2005; 73(5): 1011 - 1016. [Abstract] [Full Text] [PDF]
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M. Kanatsu-Shinohara, N. Ogonuki, T. Iwano, J. Lee, Y. Kazuki, K. Inoue, H. Miki, M. Takehashi, S. Toyokuni, Y. Shinkai, et al. Genetic and epigenetic properties of mouse male germline stem cells during long-term culture Development, September 15, 2005; 132(18): 4155 - 4163. [Abstract] [Full Text] [PDF]
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 J. C. Brodie and H. D. Humes Stem Cell Approaches for the Treatment of Renal Failure Pharmacol. Rev., September 1, 2005; 57(3): 299 - 313. [Abstract] [Full Text] [PDF]
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L. Hyslop, M. Stojkovic, L. Armstrong, T. Walter, P. Stojkovic, S. Przyborski, M. Herbert, A. Murdoch, T. Strachan, and M. Lako Downregulation of NANOG Induces Differentiation of Human Embryonic Stem Cells to Extraembryonic Lineages Stem Cells, September 1, 2005; 23(8): 1035 - 1043. [Abstract] [Full Text] [PDF]
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 P. Romagnani, F. Annunziato, F. Liotta, E. Lazzeri, B. Mazzinghi, F. Frosali, L. Cosmi, L. Maggi, L. Lasagni, A. Scheffold, et al. CD14+CD34low Cells With Stem Cell Phenotypic and Functional Features Are the Major Source of Circulating Endothelial Progenitors Circ. Res., August 19, 2005; 97(4): 314 - 322. [Abstract] [Full Text] [PDF]
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J.-L. Chew, Y.-H. Loh, W. Zhang, X. Chen, W.-L. Tam, L.-S. Yeap, P. Li, Y.-S. Ang, B. Lim, P. Robson, et al. Reciprocal Transcriptional Regulation of Pou5f1 and Sox2 via the Oct4/Sox2 Complex in Embryonic Stem Cells Mol. Cell. Biol., July 15, 2005; 25(14): 6031 - 6046. [Abstract] [Full Text] [PDF]
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 H. C. Chang, H. Liu, J. Zhang, J. Grifo, and L. C. Krey Developmental incompetency of denuded mouse oocytes undergoing maturation in vitro is ooplasmic in nature and is associated with aberrant Oct-4 expression Hum. Reprod., July 1, 2005; 20(7): 1958 - 1968. [Abstract] [Full Text] [PDF]
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 C. Zechel Requirement of Retinoic Acid Receptor Isotypes {alpha}, {beta}, and {gamma} during the Initial Steps of Neural Differentiation of PCC7 Cells Mol. Endocrinol., June 1, 2005; 19(6): 1629 - 1645. [Abstract] [Full Text] [PDF]
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J. Lee, B. K. Rhee, G.-Y. Bae, Y.-M. Han, and J. Kim Stimulation of Oct-4 Activity by Ewing's Sarcoma Protein Stem Cells, June 1, 2005; 23(6): 738 - 751. [Abstract] [Full Text] [PDF]
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P. Gu, B. Goodwin, A. C.-K. Chung, X. Xu, D. A. Wheeler, R. R. Price, C. Galardi, L. Peng, A. M. Latour, B. H. Koller, et al. Orphan Nuclear Receptor LRH-1 Is Required To Maintain Oct4 Expression at the Epiblast Stage of Embryonic Development Mol. Cell. Biol., May 1, 2005; 25(9): 3492 - 3505. [Abstract] [Full Text] [PDF]
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D. Strumpf, C.-A. Mao, Y. Yamanaka, A. Ralston, K. Chawengsaksophak, F. Beck, and J. Rossant Cdx2 is required for correct cell fate specification and differentiation of trophectoderm in the mouse blastocyst Development, May 1, 2005; 132(9): 2093 - 2102. [Abstract] [Full Text] [PDF]
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S.-K. Kim, M. R. Suh, H. S. Yoon, J. B. Lee, S. K. Oh, S. Y. Moon, S.-H. Moon, J. Y. Lee, J. H. Hwang, W. J. Cho, et al. Identification of Developmental Pluripotency Associated 5 Expression in Human Pluripotent Stem Cells Stem Cells, April 1, 2005; 23(4): 458 - 462. [Abstract] [Full Text] [PDF]
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M. Kanatsu-Shinohara, H. Miki, K. Inoue, N. Ogonuki, S. Toyokuni, A. Ogura, and T. Shinohara Long-Term Culture of Mouse Male Germline Stem Cells Under Serum-or Feeder-Free Conditions Biol Reprod, April 1, 2005; 72(4): 985 - 991. [Abstract] [Full Text] [PDF]
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W. A. Kues, B. Petersen, W. Mysegades, J. W. Carnwath, and H. Niemann Isolation of Murine and Porcine Fetal Stem Cells from Somatic Tissue Biol Reprod, April 1, 2005; 72(4): 1020 - 1028. [Abstract] [Full Text] [PDF]
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H. Zaehres, M. W. Lensch, L. Daheron, S. A. Stewart, J. Itskovitz-Eldor, and G. Q. Daley High-Efficiency RNA Interference in Human Embryonic Stem Cells Stem Cells, March 1, 2005; 23(3): 299 - 305. [Abstract] [Full Text] [PDF]
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G. Cauffman, H. Van de Velde, I. Liebaers, and A. Van Steirteghem Oct-4 mRNA and protein expression during human preimplantation development Mol. Hum. Reprod., March 1, 2005; 11(3): 173 - 181. [Abstract] [Full Text] [PDF]
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M. Vejlsted, B. Avery, M. Schmidt, T. Greve, N. Alexopoulos, and P. Maddox-Hyttel Ultrastructural and Immunohistochemical Characterization of the Bovine Epiblast Biol Reprod, March 1, 2005; 72(3): 678 - 686. [Abstract] [Full Text] [PDF]
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S. Okumura-Nakanishi, M. Saito, H. Niwa, and F. Ishikawa Oct-3/4 and Sox2 Regulate Oct-3/4 Gene in Embryonic Stem Cells J. Biol. Chem., February 18, 2005; 280(7): 5307 - 5317. [Abstract] [Full Text] [PDF]
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 M.-H. Tai, C.-C. Chang, L.K. Olson, and J. E. Trosko Oct4 expression in adult human stem cells: evidence in support of the stem cell theory of carcinogenesis Carcinogenesis, February 1, 2005; 26(2): 495 - 502. [Abstract] [Full Text] [PDF]
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T. P. Zwaka and J. A. Thomson A germ cell origin of embryonic stem cells? Development, January 15, 2005; 132(2): 227 - 233. [Abstract] [Full Text] [PDF]
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 M. A. Vodyanik, J. A. Bork, J. A. Thomson, and I. I. Slukvin Human embryonic stem cell-derived CD34+ cells: efficient production in the coculture with OP9 stromal cells and analysis of lymphohematopoietic potential Blood, January 15, 2005; 105(2): 617 - 626. [Abstract] [Full Text] [PDF]
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K. S. O'Shea Self-renewal vs. Differentiation of Mouse Embryonic Stem Cells Biol Reprod, December 1, 2004; 71(6): 1755 - 1765. [Abstract] [Full Text] [PDF]
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H. Kubota, M. R. Avarbock, and R. L. Brinster Growth factors essential for self-renewal and expansion of mouse spermatogonial stem cells PNAS, November 23, 2004; 101(47): 16489 - 16494. [Abstract] [Full Text] [PDF]
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 E. Bieberich, J. Silva, G. Wang, K. Krishnamurthy, and B. G. Condie Selective apoptosis of pluripotent mouse and human stem cells by novel ceramide analogues prevents teratoma formation and enriches for neural precursors in ES cell-derived neural transplants J. Cell Biol., November 22, 2004; 167(4): 723 - 734. [Abstract] [Full Text] [PDF]
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S. Kurosaka, S. Eckardt, and K. J. McLaughlin Pluripotent Lineage Definition in Bovine Embryos by Oct4 Transcript Localization Biol Reprod, November 1, 2004; 71(5): 1578 - 1582. [Abstract] [Full Text] [PDF]
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G. Pan, B. Qin, N. Liu, H. R. Scholer, and D. Pei Identification of a Nuclear Localization Signal in OCT4 and Generation of a Dominant Negative Mutant by Its Ablation J. Biol. Chem., August 27, 2004; 279(35): 37013 - 37020. [Abstract] [Full Text] [PDF]
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K. A. Hohenstein and D. H. Shain Changes in Gene Expression at the Precursor -> Stem Cell Transition in Leech Stem Cells, July 1, 2004; 22(4): 514 - 521. [Abstract] [Full Text] [PDF]
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H. M. Xu, B. Liao, Q. J. Zhang, B. B. Wang, H. Li, X. M. Zhong, H. Z. Sheng, Y. X. Zhao, Y. M. Zhao, and Y. Jin Wwp2, an E3 Ubiquitin Ligase That Targets Transcription Factor Oct-4 for Ubiquitination J. Biol. Chem., May 28, 2004; 279(22): 23495 - 23503. [Abstract] [Full Text] [PDF]
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Y. Guo, L. Einhorn, M. Kelley, K. Hirota, J. Yodoi, R. Reinbold, H. Scholer, H. Ramsey, and R. Hromas Redox Regulation of the Embryonic Stem Cell Transcription Factor Oct-4 by Thioredoxin Stem Cells, May 1, 2004; 22(3): 259 - 264. [Abstract] [Full Text] [PDF]
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R. R. Pochampally, J. R. Smith, J. Ylostalo, and D. J. Prockop Serum deprivation of human marrow stromal cells (hMSCs) selects for a subpopulation of early progenitor cells with enhanced expression of OCT-4 and other embryonic genes Blood, March 1, 2004; 103(5): 1647 - 1652. [Abstract] [Full Text] [PDF]
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E. D. Smith, Y. Xu, B. N. Tomson, C. G. Leung, Y. Fujiwara, S. H. Orkin, and J. D. Crispino More than blood, a Novel Gene Required for Mammalian Postimplantation Development Mol. Cell. Biol., February 1, 2004; 24(3): 1168 - 1173. [Abstract] [Full Text] [PDF]
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M. Kanatsu-Shinohara, S. Toyokuni, and T. Shinohara CD9 Is a Surface Marker on Mouse and Rat Male Germline Stem Cells Biol Reprod, January 1, 2004; 70(1): 70 - 75. [Abstract] [Full Text] [PDF]
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V. V. Bartsevich, J. C. Miller, C. C. Case, and C. O. Pabo Engineered Zinc Finger Proteins for Controlling Stem Cell Fate Stem Cells, November 1, 2003; 21(6): 632 - 637. [Abstract] [Full Text] [PDF]
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E. Bieberich, S. MacKinnon, J. Silva, S. Noggle, and B. G. Condie Regulation of cell death in mitotic neural progenitor cells by asymmetric distribution of prostate apoptosis response 4 (PAR-4) and simultaneous elevation of endogenous ceramide J. Cell Biol., August 4, 2003; 162(3): 469 - 479. [Abstract] [Full Text] [PDF]
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A.-R. Prusa, E. Marton, M. Rosner, G. Bernaschek, and M. Hengstschlager Oct-4-expressing cells in human amniotic fluid: a new source for stem cell research? Hum. Reprod., July 1, 2003; 18(7): 1489 - 1493. [Abstract] [Full Text] [PDF]
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Y. Tokuzawa, E. Kaiho, M. Maruyama, K. Takahashi, K. Mitsui, M. Maeda, H. Niwa, and S. Yamanaka Fbx15 Is a Novel Target of Oct3/4 but Is Dispensable for Embryonic Stem Cell Self-Renewal and Mouse Development Mol. Cell. Biol., April 15, 2003; 23(8): 2699 - 2708. [Abstract] [Full Text] [PDF]
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A. Bortvin, K. Eggan, H. Skaletsky, H. Akutsu, D. L. Berry, R. Yanagimachi, D. C. Page, and R. Jaenisch Incomplete reactivation of Oct4-related genes in mouse embryos cloned from somatic nuclei Development, April 15, 2003; 130(8): 1673 - 1680. [Abstract] [Full Text] [PDF]
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B. Li, F.-C. Yang, D. W. Clapp, and K. T. Chun Enforced expression of CUL-4A interferes with granulocytic differentiation and exit from the cell cycle Blood, March 1, 2003; 101(5): 1769 - 1776. [Abstract] [Full Text] [PDF]
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M. Buehr, J. Nichols, F. Stenhouse, P. Mountford, C.J. Greenhalgh, S. Kantachuvesiri, G. Brooker, J. Mullins, and A.G. Smith Rapid Loss of Oct-4 and Pluripotency in Cultured Rodent Blastocysts and Derivative Cell Lines Biol Reprod, January 1, 2003; 68(1): 222 - 229. [Abstract] [Full Text] [PDF]
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M. Jackson, J. W. Baird, N. Cambray, J. D. Ansell, L. M. Forrester, and G. J. Graham Cloning and Characterization of Ehox, a Novel Homeobox Gene Essential for Embryonic Stem Cell Differentiation J. Biol. Chem., October 4, 2002; 277(41): 38683 - 38692. [Abstract] [Full Text] [PDF]
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R. G. Hawley and D. A. Sobieski Stem Cell Bouillabaisse-Potpourri Stem Cells, September 1, 2002; 20(5): 360 - 363. [Full Text] [PDF]
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 D. Solter Cloning v. clowning Genes & Dev., May 15, 2002; 16(10): 1163 - 1166. [Full Text] [PDF]
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M. Boiani, S. Eckardt, H. R. Scholer, and K. J. McLaughlin Oct4 distribution and level in mouse clones: consequences for pluripotency Genes & Dev., May 15, 2002; 16(10): 1209 - 1219. [Abstract] [Full Text] [PDF]
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Y. Guo, R. Costa, H. Ramsey, T. Starnes, G. Vance, K. Robertson, M. Kelley, R. Reinbold, H. Scholer, and R. Hromas The embryonic stem cell transcription factors Oct-4 and FoxD3 interact to regulate endodermal-specific promoter expression PNAS, March 19, 2002; 99(6): 3663 - 3667. [Abstract] [Full Text] [PDF]
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