Human Recombinant TPM1-ALK, Active protein, GST Tag (V2LY-0526-LY7329)

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Basic Information

Expressed Host
Baculovirus-Insect Cells
Protein Species
Human
Tag
GST Tag
Protein Construction
This product is Human Recombinant TPM1-ALK, Active protein, GST Tag consist of Amino Acid: TPM (1-257)-ALK (1058-end) and predicts a molecular mass of 125 kDa.
Molecule Mass
125 kDa
Sequence
Amino Acid: TPM (1-257)-ALK (1058-end)
Species
Human

Formulations & Storage [For reference only, actual COA shall prevail!]

Purity
Batch dependent.
Endotoxin
Please contact us for more information.
Format
Liquid
Buffer
PBS
Preservative
None
Storage
Store product at -70°C. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles.
More Infomation

Target

Full Name
TPM1 Gene(Protein Coding) Tropomyosin 1
Function
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
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
Cellular Location
Cytoplasm, cytoskeleton
Associates with F-actin stress fibers.
Involvement in disease
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.
PTM
Phosphorylated at Ser-283 by DAPK1 in response to oxidative stress and this phosphorylation enhances stress fiber formation in endothelial cells.
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For research use only. Not intended for any clinical use.

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