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Merck
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AB5441

Sigma-Aldrich

Anti-Tropomyosin Antibody

Chemicon®, from sheep

Sinónimos:

Anti-C15orf13, Anti-CMD1Y, Anti-CMH3, Anti-HEL-S-265, Anti-HTM-alpha, Anti-LVNC9, Anti-TMSA

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About This Item

Código UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41

origen biológico

sheep

Nivel de calidad

forma del anticuerpo

affinity purified immunoglobulin

tipo de anticuerpo

primary antibodies

clon

polyclonal

purificado por

affinity chromatography

reactividad de especies

mouse, rat

fabricante / nombre comercial

Chemicon®

técnicas

immunocytochemistry: suitable
immunohistochemistry: suitable
western blot: suitable

Nº de acceso UniProt

Condiciones de envío

dry ice

modificación del objetivo postraduccional

unmodified

Información sobre el gen

Especificidad

Recognizes Tropomyosin 1, 2, 3, 5a, 5b, 6.

Inmunógeno

Synthetic peptide corresponding to the 9d exon from the alpha gene of tropomyosin.

Aplicación

Research Category
Metabolism
Research Sub Category
Muscle Physiology
This Anti-Tropomyosin Antibody is validated for use in WB, IC, IH for the detection of Tropomyosin.
Western Blot: 1:200-1:1,000. The antibody reacts with the ~29 kDa Tropomyosin protein on mouse brain cytosol. An additional band at ~52-55 kDa may be seen depending on sample and antibody concentration used. It is thought that this band may be a dimer.
Immunocytochemistry: 1:100-1:500
Immunohistochemistry: 1:100-1:500


Optimal working dilutions must be determined by the end user.

Forma física

Affinity purified immunoglobulin. Liquid in PBS.

Almacenamiento y estabilidad

Maintain at -20°C in undiluted aliquots for up to 6 months after date of receipt. Avoid repeated freeze/thaw cycles.

Información legal

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

Cláusula de descargo de responsabilidad

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 clase de almacenamiento

10 - Combustible liquids

Clase de riesgo para el agua (WGK)

WGK 2

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable


Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Eui-Jung Park et al.
American journal of physiology. Renal physiology, 304(7), F958-F971 (2013-01-11)
It has been reported that several proteins [heat shock protein 70 (Hsp70 and Hsc70), annexin II, and tropomyosin 5b] interact with the Ser(256) residue on the COOH terminus of aquaporin-2 (AQP2), where vasopressin-induced phosphorylation occurs for mediating AQP2 trafficking. However
Functional effects of mutations in the tropomyosin-binding sites of tropomodulin1 and tropomodulin3.
Lewis, RA; Yamashiro, S; Gokhin, DS; Fowler, VM
Cytoskeleton (Hoboken, N.J.) null
Sawako Yamashiro et al.
The Journal of biological chemistry, 289(17), 11616-11629 (2014-03-20)
Tropomodulins (Tmods) are F-actin pointed end capping proteins that interact with tropomyosins (TMs) and cap TM-coated filaments with higher affinity than TM-free filaments. Here, we tested whether differences in recognition of TM or actin isoforms by Tmod1 and Tmod3 contribute
Maria Sckolnick et al.
Molecular biology of the cell, 27(19), 2889-2897 (2016-08-19)
Tropomyosin (Tpm) isoforms decorate actin with distinct spatial and temporal localization patterns in cells and thus may function to sort actomyosin processes by modifying the actin track affinity for specific myosin isoforms. We examined the effect of three Tpm isoforms
Ju Lan Chun et al.
Stem cells translational medicine, 2(1), 68-80 (2013-01-04)
Duchenne muscular dystrophy (DMD) is the most common form of muscular dystrophy. DMD patients lack dystrophin protein and develop skeletal muscle pathology and dilated cardiomyopathy (DCM). Approximately 20% succumb to cardiac involvement. We hypothesized that mesoangioblast stem cells (aorta-derived mesoangioblasts

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