ZNF238

Zinc finger protein 238 (also known as RP58 or ZBTB18) is a zinc finger containing transcription factor that in humans is encoded by the ZNF238 gene.[5][6]

ZBTB18
Identifiers
AliasesZBTB18, C2H2-171, MRD22, RP58, TAZ-1, ZNF238, zinc finger and BTB domain containing 18
External IDsOMIM: 608433 MGI: 1353609 HomoloGene: 21276 GeneCards: ZBTB18
Gene location (Human)
Chr.Chromosome 1 (human)[1]
Band1q44Start244,048,939 bp[1]
End244,057,476 bp[1]
RNA expression pattern


More reference expression data
Orthologs
SpeciesHumanMouse
Entrez

10472

30928

Ensembl

ENSG00000179456

ENSMUSG00000063659

UniProt

Q99592

Q9WUK6

RefSeq (mRNA)

NM_001278196
NM_006352
NM_205768

RefSeq (protein)

NP_001265125
NP_006343
NP_991331

Location (UCSC)Chr 1: 244.05 – 244.06 MbChr 1: 177.44 – 177.45 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Function

ZNF238 is a gene that plays a major role in the "promotion of ordered and correctly timed neurogenesis leading to proper layer formation and cortical growth."[7] The loss of ZNF238 has been observed to cause microcephaly, agenesis of the corpus callosum, malformation of layers in the cerebral cortex, and cerebellar hypoplasia.[7] Additionally, its absence can cause a decrease in Ngn2 and Neurod1 (in progenitor cells, and an increase thereof in mutant neurons), with the result of less progenitor cells and an increase in neuronal differentiation and glial cell growth.[7] ZNF238 also regulates repressed genes that, if left unchecked, can lead to glioma progression. Furthermore, an absence of ZNF238 results in upregulation of the epithelial-mesenchymal transition process.

In tumors such as medulloblastomas, the loss of ZNF238 can disorganize the tumor's cellular divisional processes, resulting in a cellularly diverse neoplasm. This new diversity has been observed to increase the invasiveness of the tumor, yielding proliferation into more areas of the brain than before the loss of ZNF238.

C2H2-type zinc finger proteins, such as ZNF238, act on the molecular level as transcriptional activators or repressors and are involved in chromatin assembly.[8]

Interactions

ZNF238 has been shown to interact with DNMT3A.[9]

References

  1. GRCh38: Ensembl release 89: ENSG00000179456 - Ensembl, May 2017
  2. GRCm38: Ensembl release 89: ENSMUSG00000063659 - Ensembl, May 2017
  3. "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. Becker KG, Lee IJ, Nagle JW, Canning RD, Gado AM, Torres R, Polymeropoulos MH, Massa PT, Biddison WE, Drew PD (November 1997). "C2H2-171: a novel human cDNA representing a developmentally regulated POZ domain/zinc finger protein preferentially expressed in brain". International Journal of Developmental Neuroscience. 15 (7): 891–9. doi:10.1016/S0736-5748(97)00034-8. PMID 9568537. S2CID 37032889.
  6. Aoki K, Ishida R, Kasai M (January 1997). "Isolation and characterization of a cDNA encoding a Translin-like protein, TRAX". FEBS Letters. 401 (2–3): 109–12. doi:10.1016/S0014-5793(96)01444-5. PMID 9013868. S2CID 46704829.
  7. Xiang C, Baubet V, Pal S, Holderbaum L, Tatard V, Jiang P, et al. (April 2012). "RP58/ZNF238 directly modulates proneurogenic gene levels and is required for neuronal differentiation and brain expansion". Cell Death and Differentiation. 19 (4): 692–702. doi:10.1038/cdd.2011.144. PMC 3307985. PMID 22095278.
  8. "Entrez Gene: ZNF238 zinc finger protein 238".
  9. Fuks F, Burgers WA, Godin N, Kasai M, Kouzarides T (May 2001). "Dnmt3a binds deacetylases and is recruited by a sequence-specific repressor to silence transcription". The EMBO Journal. 20 (10): 2536–44. doi:10.1093/emboj/20.10.2536. PMC 125250. PMID 11350943.

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.

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