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Key Documents

HPA009066

Sigma-Aldrich

Anti-TPM3 antibody produced in rabbit

Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution

Sinônimo(s):

Anti-Tropomyosin α-3 chain antibody produced in rabbit, Anti-Tropomyosin γ antibody produced in rabbit, Anti-Tropomyosin-3 antibody produced in rabbit, Anti-hTM5 antibody produced in rabbit

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About This Item

Código UNSPSC:
12352203
Número do Atlas de Proteínas Humanas:
NACRES:
NA.41

fonte biológica

rabbit

conjugado

unconjugated

forma do anticorpo

affinity isolated antibody

tipo de produto de anticorpo

primary antibodies

clone

polyclonal

linha de produto

Prestige Antibodies® Powered by Atlas Antibodies

forma

buffered aqueous glycerol solution

reatividade de espécies

human, mouse, rat

técnica(s)

immunoblotting: 0.04-0.4 μg/mL
immunohistochemistry: 1:50-1:200

sequência de imunogênio

AERLQREVEGERRAREQAEAEVASLNRRIQLVEEELDRAQERLATALQKLEEAEKAADESERGMKVIENRALKDEEKMELQEIQLKEAKHIAEEADRKYEEVARKLVIIEGDLERTEERAELAESRCREMDEQIRLMDQNLKCLSA

nº de adesão UniProt

Condições de expedição

wet ice

temperatura de armazenamento

−20°C

modificação pós-traducional do alvo

unmodified

Informações sobre genes

human ... TPM3(7170)

Descrição geral

TPM3 (tropomyosin 3) gene is localized to human chromosome 1q21.3, and codes for an actin-binding protein. It is present in skeletal and smooth muscles, as well as certain non-muscular tissues. It functions as an oncogene.

Imunogênio

Tropomyosin α-3 chain recombinant protein epitope signature tag (PrEST)

Aplicação

Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Western Blotting (1 paper)

Ações bioquímicas/fisiológicas

TPM3 (tropomyosin 3) is involved in the stabilization of cytoskeleton microfilaments. Upon induction by Ca2+ in skeletal muscles, it mediates the actin-myosin response. However, its function in non-muscular cells is still not clear. TPM3-ALK (anaplastic lymphoma receptor tyrosine kinase) fusion through (1;2) translocation results in hematopoietic tumorigenesis. Fusion with NTRK1 and PDGFRB genes results in the induction of papillary thyroid carcinoma and chronic eosinophilic leukemia. It is responsible for the migration and invasion in hepatocellular carcinoma by facilitating EMT (epithelial-mesenchymal transition) in a Snail-dependent manner. Expression of this protein in tumors is positively linked with the expression of MMP (matrix metalloproteinases). Hence, this protein plays a key role in the progression of gliomas. Mutations in this gene are responsible for the neuromuscular defects in patients with congenital myopathy with fibre type disproportion (CFTD).

Características e benefícios

Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.

Every Prestige Antibody is tested in the following ways:
  • IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
  • Protein array of 364 human recombinant protein fragments.

Ligação

Corresponding Antigen APREST70731

forma física

Solution in phosphate-buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide

Informações legais

Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany

Exoneração de responsabilidade

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Código de classe de armazenamento

10 - Combustible liquids

Classe de risco de água (WGK)

WGK 1

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable

Equipamento de proteção individual

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


Certificados de análise (COA)

Busque Certificados de análise (COA) digitando o Número do Lote do produto. Os números de lote e remessa podem ser encontrados no rótulo de um produto após a palavra “Lot” ou “Batch”.

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Visite a Biblioteca de Documentos

Tao Tao et al.
Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 35(9), 9053-9059 (2014-06-11)
Recent studies have shown that many molecular mechanisms, such as the EGFR, AKT, STAT3, and beta-catenin pathways, are involved in glioma. However, the prognosis of the disease remains poor. Explorations of the underlying mechanisms of glioma and identification of effective
T Schreckenbach et al.
Neuromuscular disorders : NMD, 24(2), 117-124 (2013-11-19)
Cap myopathy is a rare congenital myopathy characterized by the presence of caps within muscle fibres and caused by mutations in ACTA1, TPM2 or TPM3. Thus far, only three cases with TPM3-related cap myopathy have been described. Here, we report
P Munot et al.
Neuromuscular disorders : NMD, 20(12), 796-800 (2010-10-19)
Congenital myopathy with fibre type disproportion (CFTD) has been associated with mutations in ACTA1, SEPN1, RYR1 and TPM3 genes. We report the clinico-pathological and electrophysiological features of 2 unrelated cases with heterozygous TPM3 mutation. Case 1 is a 19-year-old lady
D C Singleton et al.
Oncogene, 34(36), 4713-4722 (2014-12-09)
Hypoxia is a common feature of locally advanced breast cancers that is associated with increased metastasis and poorer survival. Stabilisation of hypoxia-inducible factor-1α (HIF1α) in tumours causes transcriptional changes in numerous genes that function at distinct stages of the metastatic

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