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心肌肌钙蛋白抗体Cardiac Troponin I/TNNC1troponin I type 3
产品名称:
心肌肌钙蛋白抗体Cardiac Troponin I/TNNC1troponin I type 3
英文名称:
Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
型号:
0799R
产品库存
101
产品价格
电议

产品详情

 研究领域 心血管  免疫学   

抗体来源 Rabbit 
克隆类型 Polyclonal 
交叉反应 Human, Mouse, Rat, Dog, Pig, Cow, Rabbit,  
产品应用 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500 (石蜡切片需做抗原修复)
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user. 
分 子 量 23kDa 
细胞定位 细胞浆  
性    状 Liquid 
浓    度 1mg/ml 
免 疫 原 KLH conjugated synthetic peptide derived from human CTn1:131-210/210  
亚    型 IgG 
纯化方法 affinity purified by Protein A 
储 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. 
保存条件 Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. 
PubMed PubMed 
产品介绍 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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