Connexins (Cx) are a multi-gene family of highly related proteins with molecular weights ranging from 26 to 70 kD. The structure of connexin molecules includes a cytoplasmic N-terminal region, four transmembrane domains, two extracellular loops, and a C-terminal cytoplasmic tail of varying length. Anti-Connexin 32 is developed in rabbit using synthetic peptide Lys- Arg- Ser-Pro- Gly- Thr- Gly- Ala-Gly- Leu- Ala- Glu- Lys-Ser- Asp- Arg conjugated to KLH with glutaraldehyde as immunogen.
Gap junction protein, connexin-32 (Cx32) is encoded by gap junction protein β 1 (GJB1) gene, localized on the human chromosome X. This gene is expressed in the central nervous system (CNS) in oligodendrocytes and other neuronal populations.
Immunogen
synthetic human/rat connexin-32 peptide (amino acids 265-279 with an N-terminally added lysine).
Application
Anti-Connexin-32 (265-279) antibody produced in rabbit has been used in western blot analysis and immunocytochemistry.
Biochem/physiol Actions
Mutations of the gap junction protein β 1 (GJB1) gene results in the X-linked form of Charcot-Marie-tooth disease (CMTX1). Cx32 participates in the liver regeneration after partial hepatectomy.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 1% bovine serum albumin with 15 mM sodium azide.
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Cx32 hemichannel opening by cytosolic Ca2+ is inhibited by the R220X mutation that causes Charcot-Marie-Tooth disease
Carrer A, et al.
Human Molecular Genetics, 27(1), 80-94 (2017)
An 8-generation family with X-linked Charcot-Marie-Tooth: Confirmation Of the pathogenicity Of a 3? untranslated region mutation in GJB1 and its clinical features
Pannexin1 (Panx1) subunits oligomerize to form large-pore channels between the intracellular and extracellular milieu that have been shown to regulate proliferation, differentiation and cell death mechanisms. These key cellular responses are ultimately necessary for normal tissue development and function but
Six novel connexin32 (GJB1) mutations in X-linked Charcot-Marie-Tooth disease
Lee MJ, et al.
Journal of Neurology, Neurosurgery, and Psychiatry, 73(3), 304-306 (2002)
Role of connexin (gap junction) genes in cell growth control and carcinogenesis
Yamasaki H, et al.
Comptes Rendus de l'Academie des Sciences. Serie iii, Sciences de la Vie, 322(2-3), 151-159 (1999)
Cancer research has revealed that the classical model of carcinogenesis, a three step process consisting of initiation, promotion, and progression, is not complete.
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