Tyr215
Javascript is not enabled on this browser. This site will not work properly without Javascript.
PhosphoSitePlus Homepage PhosphoSitePlus® v6.8.2
Powered by Cell Signaling Technology
Home > Phosphorylation Site Page: > Tyr215  -  cGAS (human)

Site Information
LLNTGSyyEHVKIsA   SwissProt Entrez-Gene
Blast this site against: NCBI  SwissProt  PDB 
Site Group ID: 1271626200

In vivo Characterization
Methods used to characterize site in vivo:
immunoassay ( 3 ) , mass spectrometry ( 1 ) , mutation of modification site ( 1 , 2 , 3 ) , phospho-antibody ( 1 , 3 ) , western blotting ( 1 , 3 )
Disease tissue studied:
lung cancer ( 3 ) , non-small cell lung cancer ( 3 ) , non-small cell lung adenocarcinoma ( 3 )
Relevant cell line - cell type - tissue:

Upstream Regulation
Putative in vivo kinases:
BLK (human) ( 3 ) , Syk (human) ( 1 )
Treatments:
etoposide ( 3 ) , vanadate ( 3 )

Downstream Regulation
Effects of modification on cGAS:
enzymatic activity, induced ( 1 ) , enzymatic activity, inhibited ( 2 ) , intracellular localization ( 2 , 3 ) , molecular association, regulation ( 1 , 2 )
Effects of modification on biological processes:
chromatin organization, altered ( 2 ) , DNA repair, induced ( 2 ) , DNA repair, inhibited ( 3 )
Induce interaction with:
DNA ( 1 )
Inhibit interaction with:
DNA ( 2 )

References 

1

Yang YL, et al. (2022) Endocytosis triggers V-ATPase-SYK-mediated priming of cGAS activation and innate immune response. Proc Natl Acad Sci U S A 119, e2207280119
36252040   Curated Info

2

Jiang H, et al. (2019) Chromatin-bound cGAS is an inhibitor of DNA repair and hence accelerates genome destabilization and cell death. EMBO J 38, e102718
31544964   Curated Info

3

Liu H, et al. (2018) Nuclear cGAS suppresses DNA repair and promotes tumorigenesis. Nature 563, 131-136
30356214   Curated Info