bs-70294R

DATASHEET

Host: Rabbit

Target Protein: Troponin I (cardiac) Ser23/24

Specificity: Specific for endogenous levels of the ~25 kDa cardiac troponin I protein phosphorylated at Ser23/24. Immunolabeling is blocked by preadsorption with the phosphopeptide used as antigen, but not by the corresponding non-phosphopeptide.

Modification Site: Ser23,24

Clonality: Polyclonal

Isotype: IgG

Entrez Gene: 21954

Swiss Prot: P48787

Source: Synthetic phospho-peptide corresponding to amino acid residues surrounding Ser23/24 of mouse troponin 1, cardiac (cTnI), conjugated to keyhole limpet hemocyanin (KLH).

Purification: Antigen Affinity purification from Pooled whole antiserum

Storage Buffer: 10 mM HEPES (pH 7.5), 150 mM NaCl, 100 µg per ml BSA and 50% glycerol.

Storage: Storage at -20°C is recommended, as aliquots may be taken without freeze/thawing due to presence of 50% glycerol. Stable for at least 1 year at -20°C.

Background:

Troponin I (cTnI) is 1 of 3 subunits, along with troponin C (TnC) and troponin T (TnT) of troponin complex found in cardiac muscle. cTnI binds to actin in thin myofilaments to hold the troponin-tropomyosin complex in place. Phosphorylation of cardiac isoform of TnI at serines 22,23 in the unique amino-terminal end molecule decreases the calcium sensitivity of the sarcomere, promotes calcium dissociation from troponin C and by extension enhances rates of cross-bridge cycling and diastolic relaxation (Noland, Jr. et al., 1995; Noland et al., 1989). In addition, studies using reconstituted fibers and mutational analysis have shown that PKC phosphorylation of TnI (largely at Ser-43) inhibits the actin-cross bridge reaction and reduces the Ca++ dependent actomyosin ATPase rate as well as the calcium sensitivity of force generation (Noland, Jr. and Kuo, 1991). Phosphorylation at Thr-144 (mediated by several PKC isoforms) reduces maximal tension development and cross-bridge cycling rates (Sumandea et al., 2008). Importantly, changes in the phosphorylation at each of these sites have been shown to be stage-specific with regard to cardiac disease progression (Walker et al., 2010).