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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

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

biological source

sheep

Quality Level

100

antibody form

affinity purified immunoglobulin

antibody product type

primary antibodies

clone

polyclonal

purified by

affinity chromatography

species reactivity

mouse, rat

manufacturer/tradename

Chemicon®

technique(s)

immunocytochemistry: suitable
immunohistochemistry: suitable
western blot: suitable

NCBI accession no.

NM_000366.5
NM_001018004.1
NM_001018005.1
NM_001018006.1
NM_001018007.1
NM_001018008.1
NM_001018020.1

UniProt accession no.

P09493

shipped in

dry ice

target post-translational modification

unmodified

Gene Information

rat ... Tpm3(117557)

Specificity

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

Immunogen

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

Application

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.

Physical form

Affinity purified immunoglobulin. Liquid in PBS.

Storage and Stability

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

Legal Information

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

Disclaimer

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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Storage Class

10 - Combustible liquids

wgk_germany

WGK 2

flash_point_f

Not applicable

flash_point_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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