09-881
Anti-acetyl Cortactin Antibody
from rabbit, purified by affinity chromatography
Synonym(s):
Amplaxin, Oncogene EMS1, Src substrate cortactin
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
rabbit
Quality Level
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
purified by
affinity chromatography
species reactivity
mouse, human
species reactivity (predicted by homology)
Drosophila (based on 100% sequence homology), rat (based on 100% sequence homology)
technique(s)
western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
acetylation (not specified)
Gene Information
human ... CTTN(2017)
General description
Cortactin is a cytoskeleton protein that facilitates assembly of cortical actin. Cortactin is widely expressed in most adherent cells and is a prominent substrate of protein-tyrosine kinase Src in vivo and in vitro. The protein sequence of cortactin contains multiple amino-terminal tandem repeats of a unique 37-amino acid sequence, which associates with actin, and a Src homology 3 domain at the carboxyl terminus.
Recent research efforts show cortactin is acetylated in vivo and is deacetylated by HDAC6 (Histone deacetylase 6). HDAC6 is a tubulin-specific deacetylase that regulates microtubule-dependent cell movement. In recent studies it was demonstrated that HDAC6 binds cortactin and alters the ability of cortactin to bind F-actin by modulating a “charge patch” in its repeat region. Findings suggest that, in addition to its role in microtubule-dependent cell motility, HDAC6 influences actin-dependent cell motility by altering the acetylation status of cortactin, which, in turn, changes the F-actin binding activity of cortactin. The acetylation level of cortactin may correlate to tumor metastases and acetylated cortactin may be considered a potential metastasis marker.
Recent research efforts show cortactin is acetylated in vivo and is deacetylated by HDAC6 (Histone deacetylase 6). HDAC6 is a tubulin-specific deacetylase that regulates microtubule-dependent cell movement. In recent studies it was demonstrated that HDAC6 binds cortactin and alters the ability of cortactin to bind F-actin by modulating a “charge patch” in its repeat region. Findings suggest that, in addition to its role in microtubule-dependent cell motility, HDAC6 influences actin-dependent cell motility by altering the acetylation status of cortactin, which, in turn, changes the F-actin binding activity of cortactin. The acetylation level of cortactin may correlate to tumor metastases and acetylated cortactin may be considered a potential metastasis marker.
Specificity
The antibody recognizes human acetylated Cortactin.
Immunogen
Consensus sequence motif of acetylation sites of cortactin.
Epitope: Unknown
Application
Research Category
Cell Structure
Cell Structure
Research Sub Category
Cytoskeleton
Cytoskeleton
This Anti-acetyl Cortactin Antibody is validated for use in Western Blotting, for the detection of acetyl Cortactin.
Quality
Evaluated by Western Blot in HeLa-Anti-Cortactin immunocomplex treated with TSA/Nicotinamide.
Western Blot Analysis: 2.5 µg/ml of this antibody detected Cortactin on 10 µL of HeLa-Anti-Cortactin immunocomplex treated with TSA/Nicotinamide.
Western Blot Analysis: 2.5 µg/ml of this antibody detected Cortactin on 10 µL of HeLa-Anti-Cortactin immunocomplex treated with TSA/Nicotinamide.
Target description
~ 85 kDa
Physical form
Affinity purified
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4, 150 mM NaCl) with 0.05% sodium azide.
Storage and Stability
Stable for 1 year at 2-8°C from date of receipt.
Analysis Note
Control
HeLa-Anti-Cortactin immunocomplex treated with TSA/Nicotinamide
HeLa-Anti-Cortactin immunocomplex treated with TSA/Nicotinamide
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
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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Description
Pricing
Storage Class
12 - Non Combustible Liquids
wgk_germany
WGK 1
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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Pedro Guedes-Dias et al.
Biochimica et biophysica acta, 1852(11), 2484-2493 (2015-08-25)
Striatal neurons are vulnerable to Huntington's disease (HD). Decreased levels of acetylated alpha-tubulin and impaired mitochondrial dynamics, such as reduced motility and excessive fission, are associated with HD; however, it remains unclear whether and how these factors might contribute to
Zhongying Mo et al.
Nature communications, 9(1), 1007-1007 (2018-03-10)
Dominant mutations in glycyl-tRNA synthetase (GlyRS) cause a subtype of Charcot-Marie-Tooth neuropathy (CMT2D). Although previous studies have shown that GlyRS mutants aberrantly interact with Nrp1, giving insight into the disease's specific effects on motor neurons, these cannot explain length-dependent axonal
Eugenia Meiler et al.
PloS one, 7(3), e33662-e33662 (2012-04-06)
Cortactin is a classical Src kinase substrate that participates in actin cytoskeletal dynamics by activating the Arp2/3 complex and interacting with other regulatory proteins, including FAK. Cortactin has various domains that may contribute to the assembly of different protein platforms
Kahia Messaoudi et al.
Nature communications, 8(1), 1786-1786 (2017-11-28)
Thrombocytopenia is a major side effect of a new class of anticancer agents that target histone deacetylase (HDAC). Their mechanism is poorly understood. Here, we show that HDAC6 inhibition and genetic knockdown lead to a strong decrease in human proplatelet
Gabriele Di Sante et al.
Molecular endocrinology (Baltimore, Md.), 29(2), 200-212 (2014-12-30)
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