Recognizes Human, rat and mouse Connexin 45. Due to sequence homologies, this antibody is also expected to react with canine (100% homology) Connexin 45. Other species not tested.
Immunogen
KLH-conjugated synthetic, linear peptide corresponding to human Connexin 45 near the C-terminus.
Application
Detect Connexin 45 using this Anti-Connexin 45 Antibody, near C-terminus, cytoplasmic validated for use in IP, WB, IH.
Physical form
Format: Purified
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
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Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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Journal of animal science, 88(10), 3269-3279 (2010-06-22)
During mammalian oogenesis, intercellular communication between oocytes and the surrounding follicle cells through gap junction channels is crucial for oocyte development and maturation. The channel properties of gap junctions may be affected by the composition or combination of connexins, the
Gap junction (GJ) channels have been recognized as an important mechanism for synchronizing neuronal networks. Herein, we investigated the participation of GJ channels in the pilocarpine-induced status epilepticus (SE) by analyzing electrophysiological activity following the blockade of connexins (Cx)-mediated communication.
Haplodeficient mice expressing carboxyl-terminally truncated Cx43 (K258stop/KO), instead of the wild-type Cx43 isoform, reach adulthood and reveal no abnormalities in heart morphology. Here, we have analyzed the expression of K258stop protein and the morphology of gap junctions in adult hearts
Journal of the American Heart Association, 8(8), e010823-e010823 (2019-04-05)
Background Gap junction channels made of Connexin37 (Cx37) are expressed by aortic endothelial and smooth muscle cells of hypertensive mice, as well as by the renin-secreting cells of kidneys. Methods and Results To decipher whether Cx37 has any role in
Cardiac arrhythmias are a primary contributor to sudden cardiac death, a major unmet medical need. Because right ventricular (RV) dysfunction increases the risk for sudden cardiac death, we examined responses to RV stress in mice. Among immune cells accumulated in
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