Curated Information
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Home > Curated Information Page > PubMed Id: 37460805
Ai YL, et al. (2023) Mannose antagonizes GSDME-mediated pyroptosis through AMPK activated by metabolite GlcNAc-6P. Cell Res 37460805
This page summarizes selected information from the record referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2015, 43:D512-20). To learn more about the scope of PhosphoSitePlus®, click here.
Information from this record has been curated, but not yet edited in PhosphoSitePlus® and may be incomplete.
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S80-p - ACC1 (human)
Modsite: LHIRssMsGLHLVkQ SwissProt Entrez-Gene
Orthologous residues
ACC1 (human): S80‑p, ACC1 iso2 (human): S22‑p, ACC1 iso4 (human): S117‑p, ACC1 (mouse): S79‑p, ACC1 iso2 (mouse): S117‑p, ACC1 (rat): S79‑p, ACC1 iso2 (rat): S79‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Disease tissue studied:  melanoma skin cancer
Relevant cell lines - cell types - tissues:  A375 (melanocyte)
Cellular systems studied:  cell lines
Species studied:  human
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
mannose increase
CCCP, Fe, mannose increase
mannose GFAT (human) augment treatment-induced increase GFAT1/2 KO inhibits
mannose GNPNAT1 (human) augment treatment-induced increase GNPNAT1 KO inhibits
mannose PGM3 (human) no effect upon treatment-induced increase PGM3 KO has no effect
mannose UAP1 (human) no effect upon treatment-induced increase UAP1 KO has no effect
GLCNAC-6P increase
mannose CAMKK2 (human) no effect upon treatment-induced increase CAMKK2 KO has no effect
GLCNAC-6P CAMKK2 (human) no effect upon treatment-induced increase
mannose LKB1 (human) augment treatment-induced increase LKB1 KO inhibits
GLCNAC-6P LKB1 (human) augment treatment-induced increase LKB1 KO inhibits
glucosamine no change compared to control
GlcNAc no change compared to control
monomethyl auristatin E mannose inhibit treatment-induced increase
MK8722 increase
monomethyl auristatin E MK8722 no effect upon treatment-induced increase
DON mannose inhibit treatment-induced increase

T172-p - AMPKA2 (human)
Modsite: sDGEFLRtsCGsPNy SwissProt Entrez-Gene
Orthologous residues
AMPKA2 (human): T172‑p, AMPKA2 (mouse): T172‑p, AMPKA2 (rat): T172‑p, AMPKA2 (pig): T172‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Disease tissue studied:  melanoma skin cancer
Relevant cell lines - cell types - tissues:  A375 (melanocyte), colon, kidney, liver, stomach
Cellular systems studied:  cell lines, tissue
Species studied:  human
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE LKB1 (human) genetic knockout/knockin of upstream enzyme, co-immunoprecipitation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
mannose increase
CCCP, mannose, Fe increase
mannose GFAT (human) augment treatment-induced increase GFAT1/2 KO inhibits
mannose GNPNAT1 (human) augment treatment-induced increase GNPNAT1 KO inhibits
mannose PGM3 (human) no effect upon treatment-induced increase PGM3 KO has no effect
mannose UAP1 (human) no effect upon treatment-induced increase UAP1 KO has no effect
GLCNAC-6P increase
mannose CAMKK2 (human) no effect upon treatment-induced increase CAMKK2 KO has no effect
GLCNAC-6P CAMKK2 (human) no effect upon treatment-induced increase
mannose LKB1 (human) augment treatment-induced increase LKB1 KO inhibits
GLCNAC-6P LKB1 (human) augment treatment-induced increase LKB1 KO inhibits
glucosamine no change compared to control
GlcNAc no change compared to control
monomethyl auristatin E mannose inhibit treatment-induced increase
MK8722 increase
monomethyl auristatin E MK8722 no effect upon treatment-induced increase
DON mannose inhibit treatment-induced increase

T6-p - DFNA5 (human)
Modsite: __MFAkAtRNFLREV SwissProt Entrez-Gene
Orthologous residues
DFNA5 (human): T6‑p, DFNA5 (mouse): T6‑p, DFNA5 (rat): T6‑p
Characterization
Methods used to characterize site in vivo mass spectrometry (in vitro), mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  melanoma skin cancer
Relevant cell lines - cell types - tissues:  A375 (melanocyte)
Cellular systems studied:  cell lines, tissue
Species studied:  human, mouse
Enzymes shown to modify site in vitro
Type Enzyme
KINASE AMPKA1 (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA1 (human) genetic knockout/knockin of upstream enzyme, pharmacological activator of upstream enzyme, co-immunoprecipitation
KINASE AMPKA2 (human) phospho-antibody, genetic knockout/knockin of upstream enzyme, pharmacological activator of upstream enzyme, co-immunoprecipitation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
mannose increase
metformin increase
MK8722 increase
dorsomorphin mannose inhibit treatment-induced increase
Downstream Regulation
Effect of modification (function):  molecular association, regulation, protein conformation, protein stabilization
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
CASP3 (human) Disrupts co-immunoprecipitation, pull-down assay