Sunday, March 24, 2013

IN SMALL CELL LUNG CANCER ONE CANNOT OVER-EMPHASIZE THE ROLE OF SOX2 GENE!

IT IS A GENE THAT LEADS TO ORGAN DEVELOPMENT (EYES), ANOPHTHALMIA SYNDROME, MICROPHTHALMIA, SEPTO-OPTIC DYSPLASIA
 LOCATION 3q26  (NOTE THE Q)
IF IT INVOLVES ORGAN DEVELOPMENT, REMEMBER THALIDOMID AND ANTI-ANGIOGENIC DRUGS EFFECT!

SOX2

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SRY (sex determining region Y)-box 2

PDB rendering based on 1gt0.
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols SOX2; ANOP3; MCOPS3
External IDs OMIM184429 MGI98364 HomoloGene68298 GeneCards: SOX2 Gene
RNA expression pattern
PBB GE SOX2 213721 at tn.png
PBB GE SOX2 213722 at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 6657 20674
Ensembl ENSG00000181449 ENSMUSG00000074637
UniProt P48431 P48432
RefSeq (mRNA) NM_003106 NM_011443
RefSeq (protein) NP_003097 NP_035573
Location (UCSC) Chr 3:
181.43 – 181.43 Mb
Chr 3:
34.65 – 34.65 Mb

PubMed search [1] [2]
SRY (sex determining region Y)-box 2, also known as SOX2, is a transcription factor that is essential for maintaining self-renewal, or pluripotency, of undifferentiated embryonic stem cells. Sox2 is a member of the Sox family of transcription factors, which have been shown to play key roles in many stages of mammalian development. This protein family shares highly conserved DNA binding domains known as HMG (High-mobility group) box domains containing approximately 80 amino acids. Sox2 has a critical role in maintenance of embryonic and neural stem cells and holds great promise in research involving induced pluripotency, an emerging and very promising field of regenerative medicine.[1]

Contents

Function and expression in pluripotency

LIF (Leukemia inhibitory factor) signaling, which maintains pluripotency in mouse embryonic stem cells, activates Sox2 downstream of the JAK-STAT signaling pathway and subsequent activation of Klf4 (a member of the family of Kruppel-like factors). Oct-4, Sox2 and Nanog positively regulate transcription of all pluripotency circuitry proteins in the LIF pathway.[2]In an experiment involving mouse embryonic stem cells, it was discovered that Sox2 in conjunction with Oct4, c-Myc and Klf4 were sufficient for producing induced pluripotent stem cells.[6] The discovery that expression of only four transcription factors was necessary to induce pluripotency allowed future regenerative medicine research to be conducted considering minor manipulations.
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Its association with NM1  increase its amplification.
Here you find the role of JAK-STAT pathway as prominent in SCLC.
You also find understand why this propensity to CNS metastasis
They did not say anything about MEK, the door to dedifferentiation!
It forms a complex with OCT4
and interacts with  YES1, FGF4, UTF1 and ZFP206 (By similarity)
and with  . Downstream








SRRT target that mediates the promotion of neural stem cell self-renewal (By similarity). Keeps neural cells
undifferentiated by counteracting the activity of proneural proteins and suppresses neuronal differentiation (By
similarity)







Subunit: Interacts with ZSCAN10 (By similarity). Interacts with SOX3 and FGFR1 (By similarity)
Subcellular location: Nucleus
Biotechnology: POU5F1/OCT4, SOX2, MYC/c-Myc and KLF4 are the four Yamanaka factors.

Weizmann Institute of Science 
--------------------------------------------------------------This gene lies within an intron of another gene called SOX2 overlapping transcript (SOX2OT). The importance of SOX2 and OCT4 as regulators of pluripotency has been dramatically illustrated by the demonstration that these factors together with c-Myc and Klf4 or Nanog and LIN28 can induce the dedifferentiation of somatic cells into induced pluripotent stem cells (iPS) with many of the features of embryonic stem cells, Takahashi, K. and Yamanaka, S. (2006); Wernig, M. et al. (2007) and Yu, J. et al. (2007).

  Nanog is also a very important early regulator of pluripotency. Together SOX2, OCT4 and Nanog co-regulate a growing list of downstream target genes. Target genes include YES1, FGF4, UTF1, Fbx15, Zic3 and ZFP206, but this is only a sampling of the hundreds of genes that are involved. The targets of SOX2, OCT4 and Nanog have recently been identified using time course microarray and genome-wide immunoprecipition data, Sharov, A.A, et al. (2008).
Loss of function SOX2 mutations have been linked to the rare disease microphthalmia syndrome type 3, small eye, (MCOPS3), Ragge NK, et al. (2005); Verma, A.S, and Fitzpatrick, D.R. (2007.)
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(Chen et al.) SOX2 contributes to the tumorigenesis of lung cancer cells and can be used as a diagnostic probe. In addition, obviously higher expression of oncogenes c-MYC, WNT1, WNT2, and NOTCH1,  AND YOU KNOW THAT IF YOU TOUCH THE WNT , YOU FIGHT VIGOROUSLY BREAST CANCER!  OPENING UP SOX2 AS A MAJOR TARGET IN BREAST AND LUNG CANCERS!
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IF YOU DO NOT FIND A TARGET THERAPY, DREAM AGAIN!
REMEMBER THIS WHERE ANTI-HISTONE DEACYL TRANSFERASE INHIBITOR COMES HANDY!  AND YOU GUESSED IT, SOME ANTIBIOTIC FROM FUNGI WHICH ATTACK TRANSCRIPTION FACTORS.

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