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心肌肌鈣蛋白抗體Cardiac Troponin I/TNNC1troponin I type 3

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 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 
細胞定位 細胞漿  
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 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
 
 
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