6brk
From Proteopedia
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== Function == | == Function == | ||
| - | [https://www.uniprot.org/uniprot/SAMH1_MOUSE SAMH1_MOUSE] Protein that acts both as a host restriction factor involved in defense response to virus and as a regulator of DNA end resection at stalled replication forks (By similarity). Has deoxynucleoside triphosphate (dNTPase) activity, which is required to restrict infection by viruses: dNTPase activity reduces cellular dNTP levels to levels too low for retroviral reverse transcription to occur, blocking early-stage virus replication in dendritic and other myeloid cells (PubMed: | + | [https://www.uniprot.org/uniprot/SAMH1_MOUSE SAMH1_MOUSE] Protein that acts both as a host restriction factor involved in defense response to virus and as a regulator of DNA end resection at stalled replication forks (By similarity). Has deoxynucleoside triphosphate (dNTPase) activity, which is required to restrict infection by viruses: dNTPase activity reduces cellular dNTP levels to levels too low for retroviral reverse transcription to occur, blocking early-stage virus replication in dendritic and other myeloid cells (PubMed:23872947, PubMed:23972988, PubMed:26667483, PubMed:29379009, PubMed:31548683). Likewise, suppresses LINE-1 retrotransposon activity (PubMed:26667483). In addition to virus restriction, dNTPase activity acts as a regulator of DNA precursor pools by regulating dNTP pools (By similarity). Phosphorylation at Thr-634 acts as a switch to control dNTPase-dependent and -independent functions: it inhibits dNTPase activity and ability to restrict infection by viruses, while it promotes DNA end resection at stalled replication forks (By similarity). Functions during S phase at stalled DNA replication forks to promote the resection of gapped or reversed forks: acts by stimulating the exonuclease activity of MRE11, activating the ATR-CHK1 pathway and allowing the forks to restart replication (By similarity). Its ability to promote degradation of nascent DNA at stalled replication forks is required to prevent induction of type I interferons, thereby preventing chronic inflammation (By similarity). Ability to promote DNA end resection at stalled replication forks is independent of dNTPase activity (By similarity). Enhances immunoglobulin hypermutation in B-lymphocytes by promoting transversion mutation (PubMed:29669924).[UniProtKB:Q9Y3Z3]<ref>PMID:23872947</ref> <ref>PMID:23972988</ref> <ref>PMID:26667483</ref> <ref>PMID:29379009</ref> <ref>PMID:29669924</ref> <ref>PMID:31548683</ref> |
<div style="background-color:#fffaf0;"> | <div style="background-color:#fffaf0;"> | ||
== Publication Abstract from PubMed == | == Publication Abstract from PubMed == | ||
Current revision
The SAM domain of mouse SAMHD1 is critical for its activation and regulation
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Categories: Large Structures | Mus musculus | Antonucci JM | Buzovetsky O | Ji X | Knecht KM | Tang C | Wu L | Xiong Y
