User:Diogo Andrade Nani

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==OCT4-SOX2==
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Oct4 and Sox2 are two transcription factors (TFs) involved in various roles in murine and primate cells, mainly related to the maintenance of pluripotency and self-renewal properties in embryonic stem cells. These two factors, encoded by the ''POU5F1'' (POU Class 5 Homeobox 1) and ''SOX2'' (SRY-Box Transcription Factor 2) genes, respectively, serve as reprogramming TFs and occupy the same target genes in vivo <ref>PMID:16153702</ref><ref>PMID:18555785</ref>, forming the complex OCT4-SOX2, which is the main way in which they act, although they are not obligate heterodimers in solution.
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==OCT4==
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The OCT4 transcription factor (octamer-binding transcription factor 4), also known as OCT-3, OCT3 / 4, OTF3 or NF-A3, was discovered almost three decades ago, where its use relationship with pluripotent CTE in primate and rodent species <ref name="nimbus1">PMID:25232507</ref>. This protein is encoded by the POU5F1 gene, which is located on chromosome 6 in humans and 17 in rats, and belongs to the POU family (Pit, October, Unc) of DNA-binding proteins, which regulate the expression of target genes <ref name="nimbus1"/><ref name="nimbus2">PMID:28476334</ref>. In humans, through alternative splicing, POU5F1 generates less than eight distinct RNA transcripts, these being OCT4A, OCT4B-190, OCT4B-265, OCT4B-164, OCT4B1 and more recently reported as OCT4C, OCT4C1 and OCT4B4 variants <ref name ="nimbus2"/>.
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In addition to the generated isoforms, many studies have been carried out mainly with respect to the functions of the OCT4A isoform. Studies targeting the OCT4B isoforms (190, 265 and 164) that are not able to support an automatic restoration of the CTE, but they can respond to cellular stress, whereas the functions of OCT4B1, OCT4C and OCT4C1 have not yet been clarified<ref>PMID:20333750</ref>. OCT4A is normally expressed in the early stages of embryonic development and represents one of the main regulatory factors for pluripotency and self-review of embryonic stem cells, being considered a marker of pluripotency<ref name="nimbus3">PMID:28186969</ref>. A further differentiation of CTE into cells used for different tissues depends on rapid and rapid expression of OCT4A, and these cells are differentiated remain with the OCT4A factor silenced <ref>PMID: 27788386</ref><ref>PMID:18787205</ref><ref>PMID:23653844</ref>. However, we have already documented an open expression of transcription factors such as OCT4, SOX2 and NANOG, together or controlled, lead to tumors, metastases and the greatest recurrence after use, in different types of cancer <ref name="nimbus1"/>.
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==SOX2==
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The SOX/Sox (SRY homology box) family of proteins comprises 20 individual members in man and mouse <ref>PMID:12194848</ref>, which SOX2 is the most explored. SOX proteins are principally defined by a conserved DNA-binding element, the so-called high mobility group (HMG) that relates to a transcriptional master regulator of virility (i.e., SEX determining factor Y, SRY) and thus functionally qualifies SOX/Sox proteins as DNA-binders <ref>PMID:11071752</ref><ref>PMID:31477842</ref>. While Sox proteins contribute to various cellular functionalities, reprogramming capacity is largely confined to members of the SoxB1 group (i.e., Sox1, Sox2, and Sox3)<ref>PMID:18059259</ref>. SOX2 significantly often imposes transcription modulatory in conjunction with co-factors, such as Oct3/4.
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==References==
==References==
<references />
<references />

Revision as of 22:38, 21 June 2020

Contents

OCT4-SOX2

Oct4 and Sox2 are two transcription factors (TFs) involved in various roles in murine and primate cells, mainly related to the maintenance of pluripotency and self-renewal properties in embryonic stem cells. These two factors, encoded by the POU5F1 (POU Class 5 Homeobox 1) and SOX2 (SRY-Box Transcription Factor 2) genes, respectively, serve as reprogramming TFs and occupy the same target genes in vivo [1][2], forming the complex OCT4-SOX2, which is the main way in which they act, although they are not obligate heterodimers in solution.

OCT4

The OCT4 transcription factor (octamer-binding transcription factor 4), also known as OCT-3, OCT3 / 4, OTF3 or NF-A3, was discovered almost three decades ago, where its use relationship with pluripotent CTE in primate and rodent species [3]. This protein is encoded by the POU5F1 gene, which is located on chromosome 6 in humans and 17 in rats, and belongs to the POU family (Pit, October, Unc) of DNA-binding proteins, which regulate the expression of target genes [3][4]. In humans, through alternative splicing, POU5F1 generates less than eight distinct RNA transcripts, these being OCT4A, OCT4B-190, OCT4B-265, OCT4B-164, OCT4B1 and more recently reported as OCT4C, OCT4C1 and OCT4B4 variants [4]. In addition to the generated isoforms, many studies have been carried out mainly with respect to the functions of the OCT4A isoform. Studies targeting the OCT4B isoforms (190, 265 and 164) that are not able to support an automatic restoration of the CTE, but they can respond to cellular stress, whereas the functions of OCT4B1, OCT4C and OCT4C1 have not yet been clarified[5]. OCT4A is normally expressed in the early stages of embryonic development and represents one of the main regulatory factors for pluripotency and self-review of embryonic stem cells, being considered a marker of pluripotency[6]. A further differentiation of CTE into cells used for different tissues depends on rapid and rapid expression of OCT4A, and these cells are differentiated remain with the OCT4A factor silenced [7][8][9]. However, we have already documented an open expression of transcription factors such as OCT4, SOX2 and NANOG, together or controlled, lead to tumors, metastases and the greatest recurrence after use, in different types of cancer [3].

SOX2

The SOX/Sox (SRY homology box) family of proteins comprises 20 individual members in man and mouse [10], which SOX2 is the most explored. SOX proteins are principally defined by a conserved DNA-binding element, the so-called high mobility group (HMG) that relates to a transcriptional master regulator of virility (i.e., SEX determining factor Y, SRY) and thus functionally qualifies SOX/Sox proteins as DNA-binders [11][12]. While Sox proteins contribute to various cellular functionalities, reprogramming capacity is largely confined to members of the SoxB1 group (i.e., Sox1, Sox2, and Sox3)[13]. SOX2 significantly often imposes transcription modulatory in conjunction with co-factors, such as Oct3/4.


References

  1. ↑ Boyer LA, Lee TI, Cole MF, Johnstone SE, Levine SS, Zucker JP, Guenther MG, Kumar RM, Murray HL, Jenner RG, Gifford DK, Melton DA, Jaenisch R, Young RA. Core transcriptional regulatory circuitry in human embryonic stem cells. Cell. 2005 Sep 23;122(6):947-56. doi: 10.1016/j.cell.2005.08.020. PMID:16153702 doi:http://dx.doi.org/10.1016/j.cell.2005.08.020
  2. ↑ Chen X, Xu H, Yuan P, Fang F, Huss M, Vega VB, Wong E, Orlov YL, Zhang W, Jiang J, Loh YH, Yeo HC, Yeo ZX, Narang V, Govindarajan KR, Leong B, Shahab A, Ruan Y, Bourque G, Sung WK, Clarke ND, Wei CL, Ng HH. Integration of external signaling pathways with the core transcriptional network in embryonic stem cells. Cell. 2008 Jun 13;133(6):1106-17. doi: 10.1016/j.cell.2008.04.043. PMID:18555785 doi:http://dx.doi.org/10.1016/j.cell.2008.04.043
  3. ↑ 3.0 3.1 3.2 Zeineddine D, Hammoud AA, Mortada M, Boeuf H. The Oct4 protein: more than a magic stemness marker. Am J Stem Cells. 2014 Sep 5;3(2):74-82. eCollection 2014. PMID:25232507
  4. ↑ 4.0 4.1 Malakootian M, Mirzadeh Azad F, Naeli P, Pakzad M, Fouani Y, Taheri Bajgan E, Baharvand H, Mowla SJ. Novel spliced variants of OCT4, OCT4C and OCT4C1, with distinct expression patterns and functions in pluripotent and tumor cell lines. Eur J Cell Biol. 2017 Jun;96(4):347-355. doi: 10.1016/j.ejcb.2017.03.009. Epub, 2017 Apr 10. PMID:28476334 doi:http://dx.doi.org/10.1016/j.ejcb.2017.03.009
  5. ↑ Wang X, Dai J. Concise review: isoforms of OCT4 contribute to the confusing diversity in stem cell biology. Stem Cells. 2010 May;28(5):885-93. doi: 10.1002/stem.419. PMID:20333750 doi:http://dx.doi.org/10.1002/stem.419
  6. ↑ da Silva PBG, Teixeira Dos Santos MC, Rodini CO, Kaid C, Pereira MCL, Furukawa G, da Cruz DSG, Goldfeder MB, Rocha CRR, Rosenberg C, Okamoto OK. High OCT4A levels drive tumorigenicity and metastatic potential of medulloblastoma cells. Oncotarget. 2017 Mar 21;8(12):19192-19204. doi: 10.18632/oncotarget.15163. PMID:28186969 doi:http://dx.doi.org/10.18632/oncotarget.15163
  7. ↑ Villodre ES, Kipper FC, Pereira MB, Lenz G. Roles of OCT4 in tumorigenesis, cancer therapy resistance and prognosis. Cancer Treat Rev. 2016 Dec;51:1-9. doi: 10.1016/j.ctrv.2016.10.003. Epub 2016 Oct, 14. PMID:27788386 doi:http://dx.doi.org/10.1016/j.ctrv.2016.10.003
  8. ↑ Atlasi Y, Mowla SJ, Ziaee SA, Gokhale PJ, Andrews PW. OCT4 spliced variants are differentially expressed in human pluripotent and nonpluripotent cells. Stem Cells. 2008 Dec;26(12):3068-74. doi: 10.1634/stemcells.2008-0530. Epub 2008 , Sep 11. PMID:18787205 doi:http://dx.doi.org/10.1634/stemcells.2008-0530
  9. ↑ Hatefi N, Nouraee N, Parvin M, Ziaee SA, Mowla SJ. Evaluating the expression of oct4 as a prognostic tumor marker in bladder cancer. Iran J Basic Med Sci. 2012 Nov;15(6):1154-61. PMID:23653844
  10. ↑ Schepers GE, Teasdale RD, Koopman P. Twenty pairs of sox: extent, homology, and nomenclature of the mouse and human sox transcription factor gene families. Dev Cell. 2002 Aug;3(2):167-70. doi: 10.1016/s1534-5807(02)00223-x. PMID:12194848 doi:http://dx.doi.org/10.1016/s1534-5807(02)00223-x
  11. ↑ Bowles J, Schepers G, Koopman P. Phylogeny of the SOX family of developmental transcription factors based on sequence and structural indicators. Dev Biol. 2000 Nov 15;227(2):239-55. doi: 10.1006/dbio.2000.9883. PMID:11071752 doi:http://dx.doi.org/10.1006/dbio.2000.9883
  12. ↑ Schaefer T, Lengerke C. SOX2 protein biochemistry in stemness, reprogramming, and cancer: the PI3K/AKT/SOX2 axis and beyond. Oncogene. 2020 Jan;39(2):278-292. doi: 10.1038/s41388-019-0997-x. Epub 2019 Sep, 2. PMID:31477842 doi:http://dx.doi.org/10.1038/s41388-019-0997-x
  13. ↑ Nakagawa M, Koyanagi M, Tanabe K, Takahashi K, Ichisaka T, Aoi T, Okita K, Mochiduki Y, Takizawa N, Yamanaka S. Generation of induced pluripotent stem cells without Myc from mouse and human fibroblasts. Nat Biotechnol. 2008 Jan;26(1):101-6. doi: 10.1038/nbt1374. Epub 2007 Nov 30. PMID:18059259 doi:http://dx.doi.org/10.1038/nbt1374

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