Biology:ZNF423

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Short description: Protein-coding gene in the species Homo sapiens


A representation of the 3D structure of the protein myoglobin showing turquoise α-helices.
Generic protein structure example

Zinc finger protein 423 is a protein that in humans is encoded by the ZNF423 gene.[1][2][3]

The protein encoded by this gene is a nuclear protein that belongs to the family of Kruppel-like C2H2 zinc finger proteins. It functions as a DNA-binding transcription factor by using distinct zinc fingers in different signaling pathways. Thus, it is thought that this gene may have multiple roles in signal transduction during development.[3] Mice lacking the homologous gene Zfp423 have defects in midline brain development, especially in the cerebellum,[4][5][6] as well as defects in olfactory development,[7] and adipogenesis.[8][9] Patients with mutations in ZNF423 have been reported in Joubert Syndrome and nephronophthisis.[10]

Interactions

ZNF423 has been shown to interact with EBF1,[11] PARP1,[12] Notch intracellular domain,[13] retinoic acid receptor,[14] and CEP290.[10]

References

  1. "Prediction of the coding sequences of unidentified human genes. XI. The complete sequences of 100 new cDNA clones from brain which code for large proteins in vitro". DNA Research 5 (5): 277–86. October 1998. doi:10.1093/dnares/5.5.277. PMID 9872452. 
  2. "OAZ uses distinct DNA- and protein-binding zinc fingers in separate BMP-Smad and Olf signaling pathways". Cell 100 (2): 229–40. January 2000. doi:10.1016/S0092-8674(00)81561-5. PMID 10660046. 
  3. 3.0 3.1 "Entrez Gene: ZNF423 zinc finger protein 423". https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=23090. 
  4. "Zfp423 is required for normal cerebellar development". Molecular and Cellular Biology 26 (18): 6913–22. September 2006. doi:10.1128/MCB.02255-05. PMID 16943432. 
  5. "Zfp423 controls proliferation and differentiation of neural precursors in cerebellar vermis formation". Proceedings of the National Academy of Sciences of the United States of America 103 (51): 19424–9. December 2006. doi:10.1073/pnas.0609184103. PMID 17151198. Bibcode2006PNAS..10319424A. 
  6. "The transcription factor Zfp423/OAZ is required for cerebellar development and CNS midline patterning". Developmental Biology 307 (1): 43–52. July 2007. doi:10.1016/j.ydbio.2007.04.005. PMID 17524391. 
  7. "Zfp423/OAZ participates in a developmental switch during olfactory neurogenesis". Neuron 54 (4): 547–57. May 2007. doi:10.1016/j.neuron.2007.04.029. PMID 17521568. 
  8. "Transcriptional control of preadipocyte determination by Zfp423". Nature 464 (7288): 619–23. March 2010. doi:10.1038/nature08816. PMID 20200519. Bibcode2010Natur.464..619G. 
  9. "Fetal development of subcutaneous white adipose tissue is dependent on Zfp423". Molecular Metabolism 6 (1): 111–124. January 2017. doi:10.1016/j.molmet.2016.11.009. PMID 28123942. 
  10. 10.0 10.1 "Exome capture reveals ZNF423 and CEP164 mutations, linking renal ciliopathies to DNA damage response signaling". Cell 150 (3): 533–48. August 2012. doi:10.1016/j.cell.2012.06.028. PMID 22863007. 
  11. "Cloning and functional characterization of Roaz, a zinc finger protein that interacts with O/E-1 to regulate gene expression: implications for olfactory neuronal development". The Journal of Neuroscience 17 (11): 4159–69. June 1997. doi:10.1523/jneurosci.17-11-04159.1997. PMID 9151733. 
  12. "Poly(ADP-ribose) polymerase 1 interacts with OAZ and regulates BMP-target genes". Biochemical and Biophysical Research Communications 311 (3): 702–7. November 2003. doi:10.1016/j.bbrc.2003.10.053. PMID 14623329. 
  13. "ZFP423 coordinates Notch and bone morphogenetic protein signaling, selectively up-regulating Hes5 gene expression". The Journal of Biological Chemistry 285 (40): 30814–24. October 2010. doi:10.1074/jbc.M110.142869. PMID 20547764. 
  14. "ZNF423 is critically required for retinoic acid-induced differentiation and is a marker of neuroblastoma outcome". Cancer Cell 15 (4): 328–40. April 2009. doi:10.1016/j.ccr.2009.02.023. PMID 19345331. 

Further reading

External links

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