Product Pathways - Ca / cAMP / Lipid Signaling
Gα(i) Antibody #5290
PhosphoSitePlus® protein, site, and accession data: G-alpha1(i)
| Applications | Reactivity | Sensitivity | MW (kDa) | Source |
|---|---|---|---|---|
| W | H M R | Endogenous | 40 | Rabbit |
Applications Key:
W=Western Blotting
Reactivity Key:
H=Human
M=Mouse
R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Protocols
- 5290:
- Western Blotting
Specificity / Sensitivity
Gα(i) Antibody detects endogenous levels of total Gα(i) protein.
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Arg100 of human Gα(i). Antibodies are purified by protein A and peptide affinity chromatography.
Background
Heterotrimeric guanine nucleotide-binding proteins (G proteins) consist of α, β and γ subunits and mediate the effects of hormones, neurotransmitters, chemokines and sensory stimuli. To date, over 20 known Gα subunits have been classified into four families, Gα(s), Gα(i/o), Gα(q) and Gα(12), based on structural and functional similarities (1,2). Phosphorylation of Tyr356 of Gα(q)/Gα(11) is essential for activation of the G protein, since phenylalanine substitution for Tyr356 changes the interaction of Gα with receptors and abolishes ligand-induced IP3 formation (3).
Gα(i) causes inhibition of adenylate cyclase, leading to a decrease in cellular levels of cAMP. Pertussis toxin catalyzes ADP-ribosylation of Gα(i), which inactivates the Gα(i) protein and attenuates inhibition of adenylate cyclase (4).
- Offermanns, S. (2001) Oncogene 20, 1635-42.
- Pierce, K.L. et al. (2002) Nat Rev Mol Cell Biol 3, 639-50.
- Umemori, H. et al. (1997) Science 276, 1878-81.
- Tsai, S.C. et al. (1984) J Biol Chem 259, 15320-3.
Application References
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For Research Use Only. Not For Use In Diagnostic Procedures.