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AV48224

Sigma-Aldrich

Anti-TPM2 antibody produced in rabbit

IgG fraction of antiserum

Synonym(s):

Anti-AMCD1, Anti-DA1, Anti-TMSB, Anti-TropoMyosin 2 (β)

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

IgG fraction of antiserum

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

33 kDa

species reactivity

human, rabbit, dog, rat, mouse, bovine

concentration

0.5 mg - 1 mg/mL

technique(s)

immunohistochemistry: suitable
western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... TPM2(7169)

General description

TPM2 codes for beta-tropomyosin that belongs to the actin binding protein family. Mutations in TPM2 have been linked to congenital myopathies, Sheldon-Hall syndrome and cap disease.
Rabbit anti-TPM2 antibody recognizes canine, bovine, rabbit, zebrafish, chicken, human, mouse, and rat TPM2

Immunogen

Synthetic peptide directed towards the C terminal region of human TPM2

Application

Rabbit anti-TPM2 antibodies have been used for immunoblot analysis. It is also suitable for IHC applications at a concentration of 4-8 μg/ml.

Biochem/physiol Actions

TPM2 is beta-tropomyosin, an isoform of tropomyosin that is mainly expressed in slow, type 1 muscle fibers.The TPM2 gene encodes beta-tropomyosin, an isoform of tropomyosin that is mainly expressed in slow, type 1 muscle fibers (Tajsharghi et al., 2007 [PubMed 17846275]). See also TPM1 (MIM 191010), TPM3 (MIM 191030), and TPM4 (MIM 600317).[supplied by OMIM]. Publication Note: This RefSeq record includes a subset of the publications that are available for this gene. Please see the Entrez Gene record to access additional publications.

Sequence

Synthetic peptide located within the following region: AETRAEFAERSVAKLEKTIDDLEDEVYAQKMKYKAISEELDNALNDITSL

Physical form

Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.

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 Code

10 - Combustible liquids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Minttu Marttila et al.
Human mutation, 35(7), 779-790 (2014-04-03)
Mutations affecting skeletal muscle isoforms of the tropomyosin genes may cause nemaline myopathy, cap myopathy, core-rod myopathy, congenital fiber-type disproportion, distal arthrogryposes, and Escobar syndrome. We correlate the clinical picture of these diseases with novel (19) and previously reported (31)
Vilma-Lotta Lehtokari et al.
Neuromuscular disorders : NMD, 17(6), 433-442 (2007-04-17)
"Cap myopathy" or "cap disease" is a congenital myopathy characterised by cap-like structures at the periphery of muscle fibres, consisting of disarranged thin filaments with enlarged Z discs. Here we report a deletion in the beta-tropomyosin (TPM2) gene causing cap
Jung Min Ko et al.
Journal of Korean medical science, 28(5), 780-783 (2013-05-17)
Sheldon-Hall syndrome (SHS) is a rare autosomal dominant, inherited arthrogryposis syndrome characterized by multiple congenital contractures of the distal limbs. To date, four genes that encode the skeletal muscle fiber complex have been confirmed as the causative genes. Mutations in
Carole L Moncman et al.
Experimental cell research, 319(3), 23-31 (2012-11-24)
Extraocular muscles are a unique subset of striated muscles. During postnatal development, the extraocular muscles undergo a number of myosin isoform transitions that occur between postnatal day P10 (P10) and P15. These include: (1) loss of embryonic myosin from the

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