product summary
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company name :
MyBioSource
product type :
antibody
product name :
TPM2 Antibody
catalog :
MBS9406393
quantity :
0.05 mL
price :
200 USD
clonality :
polyclonal
host :
rabbit
conjugate :
nonconjugated
reactivity :
human
application :
western blot, ELISA, immunohistochemistry, enzyme immunoassay
more info or order :
image
image 1 :
MyBioSource MBS9406393 image 1
Gel: 10%SDS-PAGE . Lysate: 40 ug Human cervical cancer tissue lysate. Primary antibody: 1/750 dilution. Secondary antibody: Goat anti Rabbit IgG - H&L (HRP). at 1/10000 dilution . Exposure time: 2 minutes
image 2 :
MyBioSource MBS9406393 image 2
The image on the left is immunohistochemistry of paraffin-embedded Human liver cancer tissue using MBS9406393 (TPM2 Antibody) at dilution 1/35, on the right is treated with the synthetic peptide.
product information
catalog number :
MBS9406393
products type :
Antibody
products full name :
TPM2 Antibody
products short name :
[TPM2]
products name syn :
[tropomyosin 2 (beta), DA1, DA2B, NEM4, TMSB, AMCD1]
other names :
[tropomyosin beta chain isoform Tpm2.1sm/cy; Tropomyosin beta chain; tropomyosin beta chain; tropomyosin 2 (beta); Beta-tropomyosin; Tropomyosin-2]
products gene name :
[TPM2]
other gene names :
[TPM2; TPM2; DA1; DA2B; NEM4; TMSB; AMCD1; HEL-S-273; TMSB]
uniprot entry name :
TPM2_HUMAN
clonality :
Polyclonal
host :
Rabbit
reactivity :
Human
sequence length :
284
specificity :
The antibody detects endogenous level of total TPM2 protein.
form :
Supplied at 1.5mg/mL in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.3, 0.05% sodium azide and 50% glycerol.
storage stability :
Store at -20°C/1 year
tested application :
ELISA (EIA), Western Blot (WB), Immunohistochemistry (IHC)
app notes :
ELISA: 1:1000-1:5000. Western blotting: 1:2000-1:5000. Immunohistochemistry: 1:50-1:200
image1 heading :
Testing Data
image2 heading :
Immunohistochemistry (IHC)
products categories :
Total protein Ab
products description :
Background: This gene encodes beta-tropomyosin, a member of the actin filament binding protein family, and mainly expressed in slow, type 1 muscle fibers. Mutations in this gene can alter the expression of other sarcomeric tropomyosin proteins, and cause cap disease, nemaline myopathy and distal arthrogryposis syndromes. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. TPM2 has been shown to interact with RRAD, PDLIM7 and TPM1.
ncbi gi num :
47519616
ncbi acc num :
NP_998839
ncbi gb acc num :
NM_213674.1
ncbi pathways :
Adrenergic Signaling In Cardiomyocytes Pathway (908257); Adrenergic Signaling In Cardiomyocytes Pathway (909696); Cardiac Muscle Contraction Pathway (93344); Cardiac Muscle Contraction Pathway (93992); Dilated Cardiomyopathy Pathway (121494); Dilated Cardiomyopathy Pathway (121285); Hypertrophic Cardiomyopathy (HCM) Pathway (114229); Hypertrophic Cardiomyopathy (HCM) Pathway (106591); Muscle Contraction Pathway (1269868); Smooth Muscle Contraction Pathway (1269870)
ncbi summary :
This gene encodes beta-tropomyosin, a member of the actin filament binding protein family, and mainly expressed in slow, type 1 muscle fibers. Mutations in this gene can alter the expression of other sarcomeric tropomyosin proteins, and cause cap disease, nemaline myopathy and distal arthrogryposis syndromes. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.[provided by RefSeq, Mar 2009]
uniprot summary :
TPM2: Binds to actin filaments in muscle and non-muscle cells. 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 is implicated in stabilizing cytoskeleton actin filaments. The non-muscle isoform may have a role in agonist-mediated receptor internalization. Defects in TPM2 are the cause of nemaline myopathy type 4 (NEM4). A form of nemaline myopathy. Nemaline myopathies are muscular disorders characterized by muscle weakness of varying severity and onset, and abnormal thread-or rod-like structures in muscle fibers on histologic examination. Nemaline myopathy type 4 presents from infancy to childhood with hypotonia and moderate-to-severe proximal weakness with minimal or no progression. Major motor milestones are delayed but independent ambulation is usually achieved, although a wheelchair may be needed in later life. Defects in TPM2 are the cause of distal arthrogryposis type 1A (DA1A). A form of distal arthrogryposis, a disease characterized by congenital joint flexures or contractures that mainly involve the distal parts of the limbs, and affect two or more different body areas in the absence of a primary neurological or muscle disease. Distal arthrogryposis type 1 is characterized largely by camptodactyly and clubfoot. Hypoplasia and/or absence of some interphalangeal creases is common. The shoulders and hips are less frequently affected. Belongs to the tropomyosin family. 3 isoforms of the human protein are produced by alternative splicing. Protein type: Motility/polarity/chemotaxis; Motor. Chromosomal Location of Human Ortholog: 9p13. Cellular Component: cytosol; muscle thin filament tropomyosin. Molecular Function: structural constituent of muscle; actin binding. Biological Process: regulation of ATPase activity; muscle contraction; muscle filament sliding. Disease: Nemaline Myopathy 4; Arthrogryposis, Distal, Type 1a; Myopathy, Congenital, With Fiber-type Disproportion; Arthrogryposis, Distal, Type 2b
size1 :
0.05 mL
price1 :
200 USD
size2 :
0.1 mL
price2 :
255
more info or order :
company information
MyBioSource
P.O. Box 153308
San Diego, CA 92195-3308
sales@mybiosource.com
https://www.mybiosource.com
1-888-627-0165
headquarters: USA
MyBioSource, LLC was orginally founded in Vancouver by three enthusiastic scientists who are passionate about providing the world with the best reagents available. Together, they form a company with a big vision known as MyBioSource. MyBioSource is now located in San Diego, California, USA.

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