Anti-CNOT7

CCR4-NOT transcription complex subunit 7(CNOT7) Homo sapiens The protein encoded by this gene binds to an anti-proliferative protein, B-cell translocation protein 1, which negatively regulates cell proliferation. Binding of the two proteins, which is driven by phosphorylation of the anti-proliferative protein, causes signaling events in cell division that lead to changes in cell proliferation associated with cell-cell contact. The encoded protein downregulates the innate immune response and therefore provides a therapeutic target for enhancing its antimicrobial activity against foreign agents. Alternative splicing of this gene results in multiple transcript variants. Related pseudogenes have been identified on chromosomes 1 and X. [provided by RefSeq, Apr 2016], Protein function: Has 3'-5' poly(A) exoribonuclease activity for synthetic poly(A) RNA substrate (PubMed:20634287, PubMed:31439799, PubMed:19276069). Its function seems to be partially redundant with that of CNOT8 (PubMed:19605561). Catalytic component of the CCR4-NOT complex which is one of the major cellular mRNA deadenylases and is linked to various cellular processes including bulk mRNA degradation, miRNA-mediated repression, translational repression during translational initiation and general transcription regulation (PubMed:20634287, PubMed:31439799, PubMed:19276069). During miRNA- mediated repression the complex seems also to act as translational repressor during translational initiation (PubMed:20065043). Additional complex functions may be a consequence of its influence on mRNA expression (PubMed:23236473, PubMed:19276069). Associates with members of the BTG family such as TOB1 and BTG2 and is required for their anti- proliferative activity (PubMed:23236473, PubMed:19276069). [The UniProt Consortium] Recommended dilutions: Western Blot: 1/500 - 1/2000. Immunohistochemistry: 1/100 - 1/300. ELISA: 1/20000. Not yet tested in other applications.. Cellular localization: Nucleus. Cytoplasm, P-body . NANOS2 promotes its localization to P-body. .