GJA1

(redirected from Cx43)
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GJA1

A gene on chromosome 6q21-q23.2 that encodes an alpha chain of the gap junction protein family, or connexins.

Molecular pathology
GJA1 mutations are associated with oculodentodigital dysplasia and cardiac malformations.
References in periodicals archive ?
About 50 [micro]g protein was separated in 12% sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and electrotransferred to PCDF membrane, and incubated with rabbit anti-human Cx43 antibody (1:1000, Santa, USA) at 37[degrees]C for 4 h, with anti-rabbit secondary antibody (1:2500, Sigma, USA) at 37[degrees]C for 2 h.
Real-time RT-PCR was performed in triplicate to analyze the expression of Cx43.
In summary, mitochondrial functional proteins play critical roles in the production of ROS in IHD: (1) the defective ETC activity, notably of decreased activity of complex I, may form the pathological foundation for mitochondria-derived ROS overload; (2) the disruption of mitochondrial dynamics, especially depressed mitochondrial fusion, will aggravate mitochondrial ROS production; (3) Tom complex may possess important property in regulating oxidative stress, perhaps via influencing the translocation of mitochondrial proteins; (4) the other functional factors, such as MPTP, MCU/MICU1/MICU2, Cx43, and STAT3, play important roles in preserving mitochondrial integrity and function, directly or indirectly through inhibiting ROS overload (Figure 1).
1 53 inflammation response miR-126 Promotion of viral SPRED1, LRP6, 55 replication and WRCH1 miR-1 Interference of cardiac Cx43 56 function miR-21 Alleviation of PDCD4 57 CVB3-induced myocarditis miR-21 and Regulation of viral ROP-yt 58 miR-146b pathogenesis miR-21 Enhancement of viral YOD1 and VCL 59 pathogenesis miR-21 Enhancement of viral SPRY1 60 pathogenesis miRNA Verified functions of the Verified Ref.
In pigs, we demonstrated that localization of Cx43 is restricted to cumulus cells, with no Cx43 detected in the oocytes, (73) and we used cell fractionation analysis to examine the cellular distribution of CD44 in COCs.
realmente realizan el efecto de expresion de las Cx43 mas que el propio
However, its breakdown is gonadotropin dependent and occurs by the clustering of Cx43 in lipid raft microdomains of the cells.
In this study, the interaction between Cx43 (the major cardiac GJ protein) and ZO-1 in rat neonatal cardiomyocytes and HeLa cells was inhibited by a peptide designed to disrupt the binding of Cx43 and ZO-1.