AUTOCAMTIDE-2-RELATED INHIBITORY PEPTIDE Chemical Properties

storage temp. 

-20°C

solubility 

H₂O: soluble

form 

lyophilized powder

color 

white

Water Solubility 

Soluble to 1 mg/ml in water

Safety Information

Hazard Codes 

Xn,F

Risk Statements 

20/21/22-36-11

Safety Statements 

22-24/25-26-36/37-16

WGK Germany 

3

MSDS

• Language:English Provider:SigmaAldrich

AUTOCAMTIDE-2-RELATED INHIBITORY PEPTIDE Usage And Synthesis

Uses

Autocamtide 2-related inhibitory peptide has been used:

• To inhibit calmodulin kinase II (CaMKII) action in virulent Theileria infected macrophages
• To study its influence on oxidative stress associated with neural cell death after hypoxia-ischemia, using neonatal hippocampal slice cultures
• To quench the phosphorylation of recombinant synGA (GTPase-activating protein) induced by CaMKII

Uses

Autocamtide-2-Related Inhibitory Peptide is a highly specific and potent inhibitor of CaMKII.

Biological Activity

synthetic peptide aip (autocamtide-2-related inhibitory peptide) is a nonphosphorylatable analog of autocamtide-2, which was identified to be a highly specific and potent inhibitor of calmodulin-dependent protein kinase ii (cam-kinase ii, camkii). camkii is a serine/threonine-specific protein kinase, which is modulated by the ca2+/calmodulin.

Biochem/physiol Actions

Calmodulin kinase II facilitates the calcium-dependent L-type calcium channels. Autocamtide 2-related inhibitory peptide action does not influence cAMP (cyclic adenosine monophosphate)-dependent protein kinase II, calmodulin-dependent protein kinase IV and protein kinase C. Increased expression of calmodulin kinase II is observed in structural heart disease, indicated by myocardial infarction. Thus, inhibition of calmodulin kinase II activity might serve as a protective effect against structural heart disease, as it is found to prevent cardiac hypertrophy, dilation and dysfunction.

in vitro

aip (1 mm) completely inhibited camkii activity, but did not affect camp-dependent protein kinase, calmodulin-dependent protein kinase iv and protein kinase c,. the inhibition was noncompetitive, and the action was caused by binding to the autophosphorylation site, which is distinc from that for the exogenous substrate. the ic50 for the autophosphorylation of cam ii is 100 nm [1].

in vivo

mice treated with aip by transgenic expression of aip, were protected from fructose-rich diet-induced arrhythmogenesis, spontaneous contractions and spontaneous ca2+ release events [2]. intra-nucleus accumbens (nac) injection of aip could dose-dependently increase the hwl (hindpaw withdrawal latency) to noxious thermal and mechanical stimulation in rats with mononeuropathy [3].

IC 50

40 nm for cam-kinase ii [1].

storage

Store at -20°C

References

[1] ishida a1, kameshita i, okuno s, kitani t, fujisawa h. a novel highly specific and potent inhibitor of calmodulin-dependent protein kinase ii. biochem biophys res commun. 1995 jul 26;212(3):806-12.
[2] sommese l, valverde ca, blanco p, castro mc, rueda ov, kaetzel m, dedman j, anderson me, mattiazzi a, palomeque j. ryanodine receptor phosphorylation by camkii promotes spontaneous ca(2+) release events in a rodent model of early stage diabetes: the arrhythmogenic substrate. int j cardiol. 2016 jan 1;202:394-406.
[3] bian h, yu lc. intra-nucleus accumbens administration of the calcium/calmodulin-dependent protein kinase ii inhibitor aip induced antinociception in rats with mononeuropathy. neurosci lett. 2015 jul 10;599:129-32.

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