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Mouse Anti-TPM1 Recombinant Antibody (CBYJT-4339) (CBMAB-T3824-YJ)


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Summary

Host Animal
Mouse
Specificity
Chicken, Human, Rat
Clone
CBYJT-4339
Antibody Isotype
IgG1, κ
Application
IF, IHC-P

Basic Information

Immunogen
Tropomyosin protein purified from chicken embryo fibroblasts (CEF) and chicken leg, heart, and gizzard
Specificity
Chicken, Human, Rat
Antibody Isotype
IgG1, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

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

Buffer
10 mM PBS, pH 7.4, 0.2% BSA
Preservative
0.09% Sodium Azide
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
TPM1 Gene(Protein Coding) Tropomyosin 1
Introduction
TPM1 binds to actin filaments in muscle and non-muscle cells. It plays a central role, in association with the troponin complex, in the calcium dependent regulation of vertebrate striated muscle contraction. Smooth muscle contraction is regulated by interaction with caldesmon. In non-muscle cells it is implicated in stabilizing cytoskeleton actin filaments.
Entrez Gene ID
Human7168
Rat24851
Chicken396366
UniProt ID
HumanP09493
RatP04692
ChickenP04268
Alternative Names
alpha-fTM
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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