ZNF865
 | This article, ZNF865, has recently been created via the Articles for creation process. Please check to see if the reviewer has accidentally left this template after accepting the draft and take appropriate action as necessary.
Reviewer tools: Inform author |
| This article, ZNF865, has recently been created via the Articles for creation process. Please check to see if the reviewer has accidentally left this template after accepting the draft and take appropriate action as necessary.
Reviewer tools: Inform author |
ZNF865 [1] (also referred to as BLST [2-4]) 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 [5]. 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 [6], worse outcome measures in esophageal cancer [7], and increased incidence of musculoskeletal diseases [8].
Broadly, ZNF865 is expressed across all human cell and tissue types [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 [5,9]. Experimental data displays ZNF865 is a regulator of cellular senescence, cell cycle progression, DNA replication, DNA repair, and protein processing [8]. 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 [8].
References
[1] https://www.genecards.org/cgi-bin/carddisp.pl?gene=ZNF865
[2] Hunter Levis, Elise Stockham, Jacob Weston, Robby D. Bowles, CRISPR-activation of a Novel Gene Increases Target Gene Expression in CRISPR-activation Multiplex Upregulated Cells. Poster Presented at: BMES 2022 Annual Meeting;
[3] Hunter Levis, Elise Stockham, Jacob Weston, Robby D. Bowles, Increased Extracellular Matrix Deposition using Synergistic Multiplex CRISPR-activation of a Novel Gene in ACAN/Col2 Upregulated Adipose-Derived Stem Cells. Poster Presented at: ORS PSRS 2022 Biennial Meeting;
[4] Hunter Levis, Elise Stockham, Jacob Weston, Robby D. Bowles, Novel Gene for Amplifying Tissue Engineered Cartilage Deposition. Poster Presented at: ORS Annual Meeting;
[5] https://www.uniprot.org/uniprotkb/P0CJ78/
[6] Liu, C., Wang, Y., Li, Jw. et al. MiR-184 Mediated the Expression of ZNF865 in Exosome to Promote Procession in the PD Model. Mol Neurobiol (2023). https://doi.org/10.1007/s12035-023-03773-2
[7] Hong, K., Yang, Q., Yin, H. et al. Comprehensive analysis of ZNF family genes in prognosis, immunity, and treatment of esophageal cancer. BMC Cancer 23, 301 (2023). https://doi.org/10.1186/s12885-023-10779-5
[8] ZNF865 Regulates Senescence and Cell Cycle for Applications to Cell Engineering and Gene Therapy
Hunter Levis, Christian Lewis, Elise Stockham, Jacob Weston, Ameerah Lawal, Brandon Lawrence, Sarah E. Gullbrand, Robby D. Bowles
bioRxiv 2023.10.25.563801; doi: https://doi.org/10.1101/2023.10.25.563801
[9] https://www.proteinatlas.org/ENSG00000261221-ZNF865/subcellular#rna