C6344
Monoclonal Anti-Connexin-32 antibody produced in mouse
clone CXN-32, ascites fluid, buffered aqueous solution
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关于此项目
Conjugate:
unconjugated
Clone:
CXN-32, monoclonal
Application:
ARR, ELISA (i), IHC (f), WB
Citations:
10
biological source
mouse
conjugate
unconjugated
antibody form
ascites fluid
antibody product type
primary antibodies
clone
CXN-32, monoclonal
form
buffered aqueous solution
mol wt
antigen 27 kDa
contains
15 mM sodium azide
species reactivity
human, rat, mouse
technique(s)
immunohistochemistry (frozen sections): suitable, indirect ELISA: suitable, microarray: suitable, western blot: 1:1,000 using a mouse whole brain extract
isotype
IgG1
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Quality Level
Gene Information
human ... GJB1(2705), GJB2(2706)
mouse ... Gjb1(14618)
rat ... Gja1(24392), Gjb1(29584)
General description
Monoclonal Anti-Connexin-32 (mouse IgG1 isotype) is derived from the CXN-32 hybridoma produced by the fusion of mouse myeloma cells and splenocytes from an immunized mouse. The 27 kDa connexin protein (Connexin-32, Cx32), belongs to the connexion family of proteins. It is expressed in most tissues, even though the pattern of expression may differ in various cell types including peripheral and central nervous system.
Immunogen
synthetic connexin-32 peptide (amino acids 105-123).
Application
Monoclonal Anti-Connexin-32 antibody produced in mouse has been used in:
- enzyme linked immunosorbent assay (ELISA)
- immunoblotting
- epifuorescent microscopy
Biochem/physiol Actions
Connexin-32 low expression levels is observed in common bile duct ligation (CBDL). In addition, a combination of myelin disruption and axonal degeneration has been shown to occur with Cx32 mutations in Charcot-Marie-Tooth disease (CMTX). Monoclonal antibodies reacting specifically with Cx32, may be used in diverse cellular and molecular approaches to the study of gap junctions and their properties, and to correlate their expression pattern with physiological functions or pathological conditions.
Connexins belong to the gap junction protein family. In humans, connexin is encoded by GJB1 (gap junction protein, β 1) gene. The gap junction proteins connexin32 (Cx32), Cx37, Cx40 and Cx43 are expressed in endothelial cells and regulate vascular functions involving inflammation. The endothelial Cx32 positively regulates angiogenesis by enhancing endothelial cell tube formation and cell migration. CX32 mutation is associated with cognitive impairment and a differential degree of peripheral nerve involvement.
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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存储类别
10 - Combustible liquids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
常规特殊物品
动植物来源生物产品
此项目有
Three-dimensional binding of epidermal growth factor peptides in colonic tissues produced from rotating bioreactor
Kaeffer B, et al.
In Vitro Cellular & Developmental Biology. Animal, 38(8), 436-439 (2002)
Connexins modulate autophagosome biogenesis
Bejarano E, et al.
Nature Cell Biology, 16(5), 401-401 (2014)
Takayuki Okamoto et al.
Experimental cell research, 321(2), 133-141 (2013-12-18)
The gap junction proteins connexin32 (Cx32), Cx37, Cx40, and Cx43 are expressed in endothelial cells, and regulate vascular functions involving inflammation, vasculogenesis and vascular remodeling. Aberrant Cxs expression promotes the development of atherosclerosis which is modulated by angiogenesis; however the
What?s the function of connexin 32 in the peripheral nervous system?
Bortolozzi M
Frontiers in Molecular Neuroscience, 11 (2018)
Structural studies of N-terminal mutants of Connexin 26 and Connexin 32 using (1)H NMR spectroscopy.
Yuksel Batir et al.
Archives of biochemistry and biophysics, 608, 8-19 (2016-07-06)
Alterations in gap junctions underlie the etiologies of syndromic deafness (KID) and Charcot-Marie Tooth disease (CMTX). Functional gap junctions are composed of connexin molecules with N-termini containing a flexible turn around G12, inserting the N-termini into the channel pore allowing
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