Mouse Anti-TPM1 Antibody (CGbeta6) (CBMAB-1694CQ)

TPM1 Gene(Protein Coding) Tropomyosin 1

This gene is a member of the tropomyosin family of highly conserved, widely distributed actin-binding proteins involved in the contractile system of striated and smooth muscles and the cytoskeleton of non-muscle cells. Tropomyosin is composed of two alpha-helical chains arranged as a coiled-coil. The encoded protein is one type of alpha helical chain that forms the predominant tropomyosin of striated muscle. It binds to actin filaments in muscle and non-muscle cells and plays a central role, in association with the troponin complex, in the calcium dependent regulation of vertebrate striated muscle contraction. Diseases associated with TPM1 include Cardiomyopathy, Hypertrophic, 3 and Cardiomyopathy, Dilated, 1E. Among its related pathways are Striated Muscle Contraction and Dilated cardiomyopathy (DCM).

alpha-fTM; tropomyosin 1 (alpha)

Binds to actin filaments in muscle and non-muscle cells (PubMed:23170982).
Plays a central role, in association with the troponin complex, in the calcium dependent regulation of vertebrate striated muscle contraction (PubMed:23170982).
Smooth muscle contraction is regulated by interaction with caldesmon. In non-muscle cells is implicated in stabilizing cytoskeleton actin filaments.

Biological Process actin filament organization Source:GO_Central1 Publication
Biological Process cardiac muscle contraction Source:BHF-UCL1 Publication
Biological Process cellular response to reactive oxygen species Source:BHF-UCL1 Publication
Biological Process cytoskeleton organization Source:BHF-UCL1 Publication
Biological Process muscle contraction Source:GO_Central1 Publication
Biological Process muscle filament sliding Source:BHF-UCLBy Similarity
Biological Process negative regulation of cell migration Source:BHF-UCLBy Similarity
Biological Process negative regulation of vascular associated smooth muscle cell migration Source:BHF-UCL1 Publication
Biological Process negative regulation of vascular associated smooth muscle cell proliferation Source:BHF-UCL1 Publication
Biological Process positive regulation of ATP-dependent activity Source:BHF-UCLBy Similarity
Biological Process positive regulation of cell adhesion Source:BHF-UCLBy Similarity
Biological Process positive regulation of heart rate by epinephrine Source:BHF-UCLBy Similarity
Biological Process positive regulation of stress fiber assembly Source:BHF-UCLBy Similarity
Biological Process regulation of cell shape Source:BHF-UCL1 Publication
Biological Process regulation of heart contraction Source:ProtInc1 Publication
Biological Process regulation of muscle contraction Source:ProtInc1 Publication
Biological Process ruffle organization Source:BHF-UCLBy Similarity
Biological Process sarcomere organization Source:BHF-UCL1 Publication
Biological Process ventricular cardiac muscle tissue morphogenesis Source:BHF-UCL1 Publication
Biological Process wound healing Source:BHF-UCLBy Similarity

Cytoplasm, cytoskeleton
Associates with F-actin stress fibers.

Cardiomyopathy, familial hypertrophic 3 (CMH3):
A hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death.
Cardiomyopathy, dilated 1Y (CMD1Y):
A disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.
Left ventricular non-compaction 9 (LVNC9):
A form of left ventricular non-compaction, a cardiomyopathy due to myocardial morphogenesis arrest and characterized by a hypertrophic left ventricle, a severely thickened 2-layered myocardium, numerous prominent trabeculations, deep intertrabecular recesses, and poor systolic function. Clinical manifestations are variable. Some affected individuals experience no symptoms at all, others develop heart failure. In some cases, left ventricular non-compaction is associated with other congenital heart anomalies. LVNC9 is an autosomal dominant condition.

Phosphorylated at Ser-283 by DAPK1 in response to oxidative stress and this phosphorylation enhances stress fiber formation in endothelial cells.