Connexin 45 Antibody (Mouse mAb) [N18M22]

Application: Reactivity: Rabbit, Rat, Human, Guinea pig

Usage Information

Dilution
WB1:1000

Application
WB, IHC, IF

Reactivity
Rabbit, Rat, Human, Guinea pig

Source
Mouse Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
45 kDa ~45 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
Connexin 45 Antibody (Mouse mAb) [N18M22] detects endogenous levels of total Connexin 45 protein.

Clone
N18M22

Synonym(s)
Gap junction gamma-1 protein, Connexin-45, Gap junction alpha-7 protein, Connexin45, Connexin 45

Background
Connexin 45 (Cx45, GJC1) is a member of the connexin family of four-pass transmembrane proteins that assemble into hexameric hemichannels and intercellular gap-junction channels, providing low-resistance pathways for ions and small signaling molecules that coordinate electrical and metabolic coupling in specialized tissues, most prominently within the cardiac conduction system. Cx45 subunits contribute to homomeric and heteromeric connexons and form gap-junction channels with relatively low unitary conductance and distinct voltage-gating properties compared with Cx43 or Cx40, properties that are suited to nodal tissue where slow, decremental conduction and strong modulation by transjunctional voltage help shape impulse delay rather than rapid longitudinal spread. In the adult heart, Cx45 is strongly expressed in the sinoatrial and atrioventricular nodes and coexpressed with Cx30.2 in nodal cells, where genetic ablation of Cx45 in mice leads to reduced AV nodal conduction capacity and, when combined with loss of Cx30.2, produces even more pronounced impairment of AV conduction, demonstrating that Cx45-containing channels are required for optimal impulse propagation and that Cx45 stabilizes Cx30.2 protein levels in the conduction system. Human genetic loss-of-function mutations in GJC1 cosegregate with autosomal dominant familial atrial fibrillation, progressive AV block, sinus bradycardia, and atrial standstill; electrophysiological characterization of mutant Cx45, such as p.M235L or p.R75H, shows markedly reduced intercellular conductance and impaired dye transfer in both homomeric and heteromeric channels with Cx43 or Cx40, consistent with a dominant-negative effect on gap-junction coupling across atrial tissue. In transgenic mouse models, cardiac-restricted overexpression of Cx45 or selective up-regulation of Cx45 in the failing heart reduces Lucifer yellow transfer and alters neurobiotin permeability between ventricular myocytes, indicating remodeling toward channels with different selectivity and lower conductance. These changes increase susceptibility to inducible ventricular tachyarrhythmias without major structural defects, and in human heart failure, Cx45 protein and junctional localization are increased while Cx43 is down-regulated, a remodeling pattern predicted to slow and heterogenize conduction and promote reentry. Complete loss of Cx45 causes early embryonic lethality with cardiovascular defects and failure of proper vascular remodeling, underscoring a role in angiogenesis and early heart morphogenesis, while conditional deletion in the adult primarily disturbs nodal conduction rather than chamber myocardium, reflecting its restricted expression pattern. Cx45 is detected in smooth muscle and central nervous system cell types where it participates in specific gap-junction networks that support vascular tone, neurovascular coupling, and neuronal or glial synchronization, but mechanistic detail and direct disease links are best established for its role in atrial and AV nodal conduction, arrhythmia susceptibility, and connexin remodeling in heart failure.

Background

Connexin 45 (Cx45, GJC1) is a member of the connexin family of four-pass transmembrane proteins that assemble into hexameric hemichannels and intercellular gap-junction channels, providing low-resistance pathways for ions and small signaling molecules that coordinate electrical and metabolic coupling in specialized tissues, most prominently within the cardiac conduction system. Cx45 subunits contribute to homomeric and heteromeric connexons and form gap-junction channels with relatively low unitary conductance and distinct voltage-gating properties compared with Cx43 or Cx40, properties that are suited to nodal tissue where slow, decremental conduction and strong modulation by transjunctional voltage help shape impulse delay rather than rapid longitudinal spread. In the adult heart, Cx45 is strongly expressed in the sinoatrial and atrioventricular nodes and coexpressed with Cx30.2 in nodal cells, where genetic ablation of Cx45 in mice leads to reduced AV nodal conduction capacity and, when combined with loss of Cx30.2, produces even more pronounced impairment of AV conduction, demonstrating that Cx45-containing channels are required for optimal impulse propagation and that Cx45 stabilizes Cx30.2 protein levels in the conduction system. Human genetic loss-of-function mutations in GJC1 cosegregate with autosomal dominant familial atrial fibrillation, progressive AV block, sinus bradycardia, and atrial standstill; electrophysiological characterization of mutant Cx45, such as p.M235L or p.R75H, shows markedly reduced intercellular conductance and impaired dye transfer in both homomeric and heteromeric channels with Cx43 or Cx40, consistent with a dominant-negative effect on gap-junction coupling across atrial tissue. In transgenic mouse models, cardiac-restricted overexpression of Cx45 or selective up-regulation of Cx45 in the failing heart reduces Lucifer yellow transfer and alters neurobiotin permeability between ventricular myocytes, indicating remodeling toward channels with different selectivity and lower conductance. These changes increase susceptibility to inducible ventricular tachyarrhythmias without major structural defects, and in human heart failure, Cx45 protein and junctional localization are increased while Cx43 is down-regulated, a remodeling pattern predicted to slow and heterogenize conduction and promote reentry. Complete loss of Cx45 causes early embryonic lethality with cardiovascular defects and failure of proper vascular remodeling, underscoring a role in angiogenesis and early heart morphogenesis, while conditional deletion in the adult primarily disturbs nodal conduction rather than chamber myocardium, reflecting its restricted expression pattern. Cx45 is detected in smooth muscle and central nervous system cell types where it participates in specific gap-junction networks that support vascular tone, neurovascular coupling, and neuronal or glial synchronization, but mechanistic detail and direct disease links are best established for its role in atrial and AV nodal conduction, arrhythmia susceptibility, and connexin remodeling in heart failure.

References
https://pubmed.ncbi.nlm.nih.gov/22982984/ https://pubmed.ncbi.nlm.nih.gov/33429106/

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%