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GSK3A (mouse)

Overview GSK3A a proline-directed protein kinase of the GSK family. Implicated in the control of several regulatory proteins including glycogen synthase, Myb, and c-Jun. GSK3 and GSK3 have similar functions. GSK3 phophorylates tau, the principal component of neurofibrillary tangles in Alzheimer disease and is required for maximal production of amyloid plaque peptides by secretase. A GSK3 promoter SNP effects progression of bipolar disorder. The GSK3 inhibitor, lithium, is used to treat bipolar disorder and is seen to block plaque formation. GSK3 generally opposes the action of insulin, and GSK3 hyperactivity is thought to contribute to insulin resistant (type II) diabetes. GSK3 also negatively regulates cardiac hypertrophy. A tumor suppressor role is indicated by the oncogenic potential of stabilized -catenin mutants that lack GSK3 phosphorylation sites. Inhibitor: AR-A014418 Note: This description may include information from UniProtKB. Protein type: Protein kinase, CMGC; EC 2.7.11.26; Kinase, protein; EC 2.7.11.1; Protein kinase, Ser/Thr (non-receptor); CMGC group; GSK family; GSK subfamily Molecular Function: transferase activity; protein serine/threonine kinase activity; protein binding; transferase activity, transferring phosphorus-containing groups; tau-protein kinase activity; nucleotide binding; kinase activity; ATP binding; protein kinase activity Biological Process: glycogen metabolic process; nervous system development; cell migration; negative regulation of TOR signaling pathway; Wnt receptor signaling pathway; genetic imprinting; negative regulation of insulin receptor signaling pathway; positive regulation of peptidyl-serine phosphorylation; protein amino acid phosphorylation; negative regulation of signal transduction; negative regulation of glucose import; negative regulation of transferase activity; cellular response to insulin stimulus; carbohydrate metabolic process; positive regulation of cAMP biosynthetic process; insulin receptor signaling pathway; regulation of systemic arterial blood pressure; positive regulation of transcription from RNA polymerase II promoter; positive regulation of heart contraction; phosphorylation Reference #:  Q2NL51 (UniProtKB) Alt. Names/Synonyms: 2700086H06Rik; glycogen synthase kinase 3 alpha; Glycogen synthase kinase-3 alpha; GSK-3 alpha; Gsk3a; OTTMUSP00000023272 Gene Symbols: Gsk3a Molecular weight: 51,661 Da Basal Isoelectric point: 8.98  Predict pI for various phosphorylation states CST Pathways:  Adherens Junction Dynamics  |  Alzheimer's Disease  |  B Cell Receptor Signaling  |  ErbB/HER Signaling  |  ESC Pluripotency and Differentiation  |  Inhibition of Apoptosis  |  Insulin Receptor Signaling  |  MAPK/Erk in Growth and Differentiation  |  mTOR Signaling  |  PI3K/Akt Signaling  |  Translation: eIF4E and p70S6K  |  Wnt/ß-Catenin Signaling Protein-Specific Antibodies or siRNAs from Cell Signaling Technology®

Select Structure to View Below GSK3A 2DFM - A=98-449 (human) Substrate Sequence Logo

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	Sites Implicated In
apoptosis, induced: S21‑p cell growth, altered: S21‑p cytoskeletal reorganization: S21‑p transcription, altered: S21‑p enzymatic activity, inhibited: S21‑p protein degradation: S21‑p

	Modification Sites and Domains	Show Modification Legend
Click here to view phosphorylation modifications only

	Modification Sites in Parent Protein, Orthologs, and Isoforms	Show Modification Legend

SS  SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.	MS  MS: The number of records in which this modification site was assigned using ONLY proteomic discovery-mode mass spectrometry.			mouse
0	4		S2-p	______MsGGGPsGG
0	3		S7-p	_MsGGGPsGGGPGGs
0	2		S14-p	sGGGPGGsGRARtss
1	76		T19-p	GGsGRARtssFAEPG
0	48		S20-p	GsGRARtssFAEPGG
121	278		S21-p	sGRARtssFAEPGGG
0	7		S39-p	GGGGPGGsAsGPGGT
0	4		S41-p	GGPGGsAsGPGGTGG
0	4		T46	sAsGPGGTGGGKASV
0	2		S72-p	SGGGPSGsGGGGsGG
0	2		S77-p	SGsGGGGsGGPGAGt
0	1		T84-p	sGGPGAGtsFPPPGV
0	1		S85-p	GGPGAGtsFPPPGVK
0	1		S97	GVKLGRDSGKVTTVV
0	1		K123	EVAYTDIKVIGNGSF
0	25		Y134	NGSFGVVYQARLAET
0	3		Y197	YLNLVLEYVPETVYR
0	1		Y220	KLITPIIYIKVYMYQ
0	1		Y226	IYIKVYMYQLFRSLA
0	7		K268-u	LCDFGSAkQLVRGEP
1	1208		S278-p	VRGEPNVsyICsRYY
15	4241		Y279-p	RGEPNVsyICsRYYR
0	1108		S282-p	PNVsyICsRYYRAPE
0	111		Y284	VsyICsRYYRAPELI
0	7		Y285	syICsRYYRAPELIF
0	3		K355-u	NPNYTEFkFPQIKAH
0	1		K372-u	TKVFKSSkTPPEAIA
0	1		A487	DATTATLASSS____

	human
S2-p	______MsGGGPsGG
S7-p	_MsGGGPsGGGPGGs
S14-p	sGGGPGGsGRARtss
T19-p	GGsGRARtssFAEPG
S20-p	GsGRARtssFAEPGG
S21-p	sGRARtssFAEPGGG
S39-p	GGGGPGGsAsGPGGt
S41-p	GGPGGsAsGPGGtGG
T46-p	sAsGPGGtGGGKASV
S72-p	SGGGPGGsGGGGsGG
S77-p	GGsGGGGsGGPGAGT
T84	sGGPGAGTSFPPPGV
S85	GGPGAGTSFPPPGVK
S97-p	GVKLGRDsGKVTTVV
K123-a	EVAYTDIkVIGNGSF
Y134-p	NGSFGVVyQARLAET
Y197-p	YLNLVLEyVPETVYR
Y220-p	KLTIPILyVKVYMyQ
Y226-p	LyVKVYMyQLFRSLA
K268-u	LCDFGSAkQLVRGEP
S278-p	VRGEPNVsyICsRyy
Y279-p	RGEPNVsyICsRyyR
S282-p	PNVsyICsRyyRAPE
Y284-p	VsyICsRyyRAPELI
Y285-p	syICsRyyRAPELIF
K355-u	NPNYTEFkFPQIKAH
R371	WTKVFKSRTPPEAIA
T480-p	TDATPTLtNSS____

	rat
S2	______MSGGGPSGG
S7	_MSGGGPSGGGPGGS
S14	SGGGPGGSGRARtSs
T19-p	GGSGRARtSsFAEPG
S20	GSGRARtSsFAEPGG
S21-p	SGRARtSsFAEPGGG
S39	GGGGPGGSASGPGGT
S41	GGPGGSASGPGGTGG
T46	SASGPGGTGGGKASV
S72	SGGGPSGSGGGGSGG
S77	SGSGGGGSGGPGAGT
T84	SGGPGAGTSFPPPGV
S85	GGPGAGTSFPPPGVK
S97	GVKLGRDSGKVTTVV
K123	EVAYTDIKVIGNGSF
Y134-p	NGSFGVVyQARLAET
Y197	YLNLVLEYVPETVYR
Y220	KLIIPIIYVKVYMYQ
Y226	IYVKVYMYQLFRSLA
K268	LCDFGSAKQLVRGEP
S278-p	VRGEPNVsyICsRyY
Y279-p	RGEPNVsyICsRyYR
S282-p	PNVsyICsRyYRAPE
Y284-p	VsyICsRyYRAPELI
Y285	syICsRyYRAPELIF
K355	NPNYTEFKFPQIKAH
R371	WTKVFKSRTPPEAIA
T480	PDATPTLTNSS____

	cow
S2	______MSGGAPSGG
S7	_MSGGAPSGGGPGGS
S14	SGGGPGGSGRARTSS
T19	GGSGRARTSSFAEPG
S20	GSGRARTSSFAEPGG
S21	SGRARTSSFAEPGGG
S39	GGGGPGGSASGPGGS
S41	GGPGGSASGPGGSGG
S46	SASGPGGSGGGKTSV
S72	SGGGPGGSGGGGSGG
S77	GGSGGGGSGGPGAGT
T84	SGGPGAGTSFPPPGV
S85	GGPGAGTSFPPPGVK
S97	GVKLGRDSGKVTTVV
K123	EVAYTDIKVIGSGSF
Y134	SGSFGVVYQARLADT
Y197	YLNLVLEYVPETVYR
Y220	KLSIPIIYVKVYMYQ
Y226	IYVKVYMYQLFRSLA
K268	LCDFGSAKQLVRGEP
S278	VRGEPNVSYICSRYY
Y279	RGEPNVSYICSRYYR
S282	PNVSYICSRYYRAPE
Y284	VSYICSRYYRAPELI
Y285	SYICSRYYRAPELIF
K355	NPNYTEFKFPQIKAH
R371	WTKVFKSRTPPEAIA
P480	TDNTATLPPGLHLLQ

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