ZNF865[5] (also referred to as BLST [2-4][6]) is a C2H2 member of the zinc finger family of proteins. Structurally, ZNF865 consists of 20 different zinc finger domains, 6 disordered regions, 2 transactivation domains, and 2 TGEKP domains.[7] Diseases associated with ZNF865 expression include Parkinson’s disease, esophageal cancer, and musculoskeletal diseases. Lack of expression of ZNF865 has been associated with increased incidence of Parkinson’s disease,[8] worse outcome measures in esophageal cancer,[8] and increased incidence of musculoskeletal diseases.
Broadly, ZNF865 is expressed across all human cell and tissue types.[7][9] Bioinformatics analysis predicts ZNF865 to be localized to the nucleus, and function in metal ion binding, DNA-binding transcription factor activity, interact with RNA polymerase II, and regulate transcription by RNA polymerase II.[9] Experimental data displays ZNF865 is a regulator of cellular senescence, cell cycle progression, DNA replication, DNA repair, and protein processing.[10][11] Lack of expression of ZNF865 induces cellular senescence, indicating that ZNF865 expression is necessary for healthy cell function. While increased expression of ZNF865 results in a shift in the cell cycle, increased rates of DNA replication and proliferation rates. Overall, ZNF865 has been confirmed as a regulator of cellular senescence, cell cycle progression, and DNA replication.[12]
References
- ^ a b c GRCh38: Ensembl release 89: ENSG00000261221 – Ensembl, May 2017
- ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000074405 – Ensembl, May 2017
- ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ "ZNF865".
- ^ Levis, Hunter; Lewis, Christian; Fainor, Matthew; Lawal, Ameerah; Stockham, Elise; Weston, Jacob; Farhang, Niloofar; Gullbrand, Sarah E.; Bowles, Robby D. (2024-11-08). "Targeted CRISPR regulation of ZNF865 enhances stem cell cartilage deposition, tissue maturation rates, and mechanical properties in engineered intervertebral discs". Acta Biomaterialia. doi:10.1016/j.actbio.2024.11.007. ISSN 1742-7061.
- ^ a b "UniProt". www.uniprot.org.
- ^ a b Hong K, Yang Q, Yin H, Wei N, Wang W, Yu B (April 2023). "Comprehensive analysis of ZNF family genes in prognosis, immunity, and treatment of esophageal cancer". BMC Cancer. 23 (1): 301. doi:10.1186/s12885-023-10779-5. PMC 10069130. PMID 37013470.
- ^ a b "Subcellular - ZNF865 - The Human Protein Atlas". www.proteinatlas.org.
- ^ Levis H, Lewis C, Stockham E, Weston JD, Lawal A, Lawrence B, Gullbrand SE, Bowles RD (2023-10-29), ZNF865 Regulates Senescence and Cell Cycle for Applications to Cell Engineering and Gene Therapy, doi:10.1101/2023.10.25.563801, S2CID 264935945, retrieved 2024-01-12
- ^ Levis, Hunter; Lewis, Christian; Fainor, Matthew; Lawal, Ameerah; Stockham, Elise; Weston, Jacob; Farhang, Niloofar; Gullbrand, Sarah E.; Bowles, Robby D. (2024-11-08). "Targeted CRISPR regulation of ZNF865 enhances stem cell cartilage deposition, tissue maturation rates, and mechanical properties in engineered intervertebral discs". Acta Biomaterialia. doi:10.1016/j.actbio.2024.11.007. ISSN 1742-7061.
- ^ Levis, Hunter; Lewis, Christian; Fainor, Matthew; Lawal, Ameerah; Stockham, Elise; Weston, Jacob; Farhang, Niloofar; Gullbrand, Sarah E.; Bowles, Robby D. (2024-11-08). "Targeted CRISPR regulation of ZNF865 enhances stem cell cartilage deposition, tissue maturation rates, and mechanical properties in engineered intervertebral discs". Acta Biomaterialia. doi:10.1016/j.actbio.2024.11.007. ISSN 1742-7061.