研究領(lǐng)域 心血管  免疫學(xué)   

抗體來源 Rabbit 

克隆類型 Polyclonal 

交叉反應(yīng) Human, Mouse, Rat, Dog, Pig, Cow, Rabbit,  

產(chǎn)品應(yīng)用 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500 （石蠟切片需做抗原修復(fù)）

not yet tested in other applications.

optimal dilutions/concentrations should be determined by the end user. 

分 子 量 23kDa 

細(xì)胞定位 細(xì)胞漿  

性    狀 Liquid 

濃    度 1mg/ml 

免 疫 原 KLH conjugated synthetic peptide derived from human CTn1:131-210/210  

亞    型 IgG 

純化方法 affinity purified by Protein A 

儲(chǔ) 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. 

保存條件 Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. 

PubMed PubMed 

產(chǎn)品介紹 Troponin I (TnI), along with troponin T (TnT) and troponin C (TnC), is one of 3 subunits that form the troponin complex of the thin filaments of striated muscle. TnI is the inhibitory subunit; blocking actin-myosin interactions and thereby mediating striated muscle relaxation. The TnI subfamily contains three genes: TnI-skeletal-fast-twitch, TnI-skeletal-slow-twitch, and TnI-cardiac. This gene encodes the TnI-cardiac protein and is exclusively expressed in cardiac muscle tissues. Mutations in this gene cause familial hypertrophic cardiomyopathy type 7 (CMH7) and familial restrictive cardiomyopathy (RCM). [provided by RefSeq, Jul 2008]

 

Function:

Troponin I is the inhibitory subunit of troponin, the thin filament regulatory complex which confers calcium-sensitivity to striated muscle actomyosin ATPase activity.

 

Subunit:

Binds to actin and tropomyosin. Interacts with TRIM63. Interacts with STK4/MST1.

 

Post-translational modifications:

Phosphorylated at Ser-42 and Ser-44 by PRKCE; phosphorylation increases myocardium contractile dysfunction. Phosphorylated at Ser-23 and Ser-24 by PRKD1; phosphorylation reduces myofilament calcium sensitivity. Phosphorylated preferentially at Thr-31. Phosphorylation by STK4/MST1 alters its binding affinity to TNNC1 (cardiac Tn-C) and TNNT2 (cardiac Tn-T).

 

DISEASE:

Defects in TNNI3 are the cause of familial hypertrophic cardiomyopathy type 7 (CMH7) [M