Recombinant Human Gap Junction Alpha-5 Protein (GJA5) Protein (His)

Name: Recombinant Human Gap Junction Alpha-5 Protein (GJA5) Protein (His)
Brand: Beta LifeScience
SKU: BLC-00556P
Availability: InStock

Greater than 85% as determined by SDS-PAGE.

Collections: High-quality recombinant proteins, Other recombinant proteins

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Product Overview

Description	Recombinant Human Gap Junction Alpha-5 Protein (GJA5) Protein (His) is produced by our E.coli expression system. This is a protein fragment.
Purity	Greater than 85% as determined by SDS-PAGE.
Uniprotkb	P36382
Target Symbol	GJA5
Synonyms	(Connexin-40)(Cx40)
Species	Homo sapiens (Human)
Expression System	E.coli
Tag	C-6His
Target Protein Sequence	YHLGWKKIRQRFVKPRQHMAKCQLSGPSVGIVQSCTPPPDFNQCLENGPGGKFFNPFSNNMASQQNTDNLVTEQVRGQEQTPGEGFIQVRYGQKPEVPNGVSPGHRLPHGYHSDKRRLSKASSKARSDDLSV
Expression Range	227-358aa
Protein Length	Partial
Mol. Weight	21.6 kDa
Research Area	Others
Form	Liquid or Lyophilized powder
Buffer	Liquid form: default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution	Briefly centrifuged the vial prior to opening to bring the contents to the bottom. Reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL. It is recommended to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. The default final concentration of glycerol is 50%.
Storage	1. Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. 2. Avoid repeated freeze-thaw cycles. 3. Store working aliquots at 4°C for up to one week. 4. In general, protein in liquid form is stable for up to 6 months at -20°C/-80°C. Protein in lyophilized powder form is stable for up to 12 months at -20°C/-80°C.
Notes	Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.

Target Details

Target Function	One gap junction consists of a cluster of closely packed pairs of transmembrane channels, the connexons, through which materials of low MW diffuse from one cell to a neighboring cell.
Subcellular Location	Cell membrane; Multi-pass membrane protein. Cell junction, gap junction.
Protein Families	Connexin family, Alpha-type (group II) subfamily
Database References	HGNC: 4279 OMIM: 108770 KEGG: hsa:2702 STRING: 9606.ENSP00000271348 UniGene: PMID: 29587382 GJA5 gene rs35594137 polymorphism is significantly associated with sudden cardiac death in the examined group. PMID: 28577096 Missense polymorphism in GJA5 independently associated with increased risk for Complete heart block after surgical repair of Congenital Heart Disease. PMID: 27826129 Cx40 genetic polymorphisms increase atrial fibrillation risk in Uyghur and Han residents of Xinjiang. PMID: 27813566 Cx 40 (rs35594137) was associated with atrial fibrillation; in the Uygur population, Cx 40 (rs35594137) should be considered as an independent risk factor for patients with atrial fibrillation, who might have racial differences in rs35594137 variant frequencies PMID: 26634538 This is a review summarizing atrial fibrillation-linked somatic and germline mutations in the gene encoding Cx40. Multiple impairments were observed in these mutants, including impaired gap junction function by abnormal localization or function, as well as increased hemichannel function. PMID: 24656738 Human atrial myocytes express Cx40 and Cx43. However, in vitro expression study indicates that human Cx40 is not able to dock with Cx43 to form heterotypic gap junction channels. This study designed two Cx40 variants, D55N or P193Q. Both of them were successful in forming functional heterotypic gap junction channels with Cx43. PMID: 26625713 Two polymorphisms in the Cx40 promoter are associated with hypertension and left ventricular hypertrophy preferentially in men. PMID: 25992486 Report interaction between ALK1 signaling and connexin40 in the development of arteriovenous malformations. PMID: 26821948 Reduced Cx40 levels and heterogeneity of its distribution (relative to Cx43) are common in atrial fibrillation. PMID: 25200600 Two atrial fibrillation-linked germline Cx40 mutants, V85I and L221I, were investigated. PMID: 24733048 Degradation of a connexin40 mutant linked to atrial fibrillation is accelerated. PMID: 24973497 These findings provide evidence that the connexin 40 Q49X mutant is capable of impairing gap-junction distribution and function of key atrial connexins, which might play a role in the predisposition to and onset of atrial fibrillation. PMID: 24626989 heterozygous Cx40A96S mice exhibit prolonged episodes of induced atrial fibrillation and severely reduced atrial conduction velocities similar to the corresponding human patient. PMID: 24060583 4 novel heterozygous GJA5 mutations, p.K107R, p.L223M, p.Q236H and p.I257L, were identified in 4 of 310 unrelated AF patients. PMID: 23292621 the germline familial mutations in Cx40 impair the gap junctions through different mechanisms, which may predispose the mutant carriers to AF. PMID: 23348765 Presence of the Cx40 minor allele (-44 G --> A) results in a uniform down-regulation of right atrial appendage Cx40 protein which was not significantly related to development of post-operative AF. PMID: 22423256 Pro265Ser variant in the carboxyl-terminus of connexin 40 alters GAP junctions and increases risk for tetralogy of Fallot. PMID: 22713807 Genotyping of rs10465885 showed that the patients with early-onset lone AF were more likely to carry the A allele compared with controls (odds ratio = 1.30; P = 0.011). PMID: 23040431 Cx40 coding SNPs are uncommon in atrial fibrillation populations, although rare mutations in this gene may lead to atrial fibrillation pathogenesis. PMID: 23134779 Results implicate GJA5 as the gene responsible for the congenital heart disease phenotypes observed with copy number imbalances at this locus. PMID: 22199024 our study could not detect an association of Cx40 promoter polymorphisms and CAD in human PMID: 22405441 This is the first evidence of intrinsic differences in the Ca2+ regulatory properties of Cx43 and Cx40. PMID: 22422398 Heteromeric cotransfection of Cx40-WT and Cx40-Q58L resulted in homogenous distribution of proteins in the plasma membrane rather than in membrane plaques in approximately 50% of cells; well-defined gap junctions were observed in other cells. PMID: 22247482 Regulation of endothelial connexin40 expression by shear stress via PI3K/Akt pathway. PMID: 22021330 Association between hereditary sick sinus node syndrome and connexin 40 gene polymorphism was demonstrated. PMID: 21649591 There is an alternate promoter polymorphism that directly affects levels of Cx40 mRNA in vivo and is associated with early-onset lone atrial fibrillation. PMID: 21076161 Three novel connexin40 mutations (p.V85I, p.L221I, and p.L229M) were identified which co-segregated with atrial fibrillation and were absent in the controls without atrial fibrillation. PMID: 20650941 In patients with cerebral ischemic events, without prior CVD, a higher prevalence of the Cx40 gene polymorphism, as a marker of underlying idiopathic atrial fibrillation appeared to be absent. PMID: 19494781 Data suggest that these dynamic changes of connexins 43, 40 and 45 during mouse cardiac development appear to be mirrored in the human. PMID: 12064615 Our data show that the presence of Cx40 does not allow GJIC and is associated with the extravillous phenotype PMID: 12397213 endothelial gap junction protein connexin 37 and connexin 40-mediated communication in the development and/or functional maintenance of segments of the mouse vasculature. PMID: 12435353 505 CHD cases were screened for the Cx40 gene to see if altered copy number associated with a cardiac phenotype. 3 cases carred deletions on chromosome 1q21.1 spanning ACPL1, Cx40, and Cx50 genes, with aortic arch anomalies being a particular feature. PMID: 15117819 The -44A allele & -44AA genotype were significantly more frequent in subjects with prior AF than in those without, providing strong evidence linking Cx40 polymorphisms to enhanced atrial vulnerability and increased risk of AF. PMID: 15297374 Coinheritance of Cx40 polymorphisms is a possible genetic factor that modifies the clinical manifestation of this inherited arrhythmia. PMID: 16188595 We conclude that decidual secretion of growth factors, such as EGF, may act to prime trophoblast for migration/invasion through modulation of connexin expression and function. PMID: 16545451 there may be more than one conformation form of the connexin40 carboxyl tail with roles in atrial conduction and arrhythmogenesis PMID: 16600287 Cx40 polymorphisms are associated with enhanced spacial dispersion of refractoriness and thus with susceptibility to reentry and atrial fibrillation PMID: 16646598 Four novel heterozygous missense mutations were identified in 4 of the 15 patients. Mutations in GJA5 may predispose patients to idiopathic atrial fibrillation by impairing gap-junction assembly or electrical coupling. PMID: 16790700 The two SNPs in the promoter region of the Cx40 gene were significantly associated with atrial fibrillation and the Cx40 (-44A +71G) haplotype was associated with a higher risk for atrial fibrillation. PMID: 16814413 a cross-talk between CFTR and a variety of gap junction channels. Cytoskeletal scaffolding proteins and/or other intermediate cytoplasmic proteins are likely to play a role in CFTR-connexins interaction. PMID: 17546509

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Proteins are sensitive to heat, and freeze-drying can preserve the activity of the majority of proteins. It improves protein stability, extends storage time, and reduces shipping costs. However, freeze-drying can also lead to the loss of the active portion of the protein and cause aggregation and denaturation issues. Nonetheless, these adverse effects can be minimized by incorporating protective agents such as stabilizers, additives, and excipients, and by carefully controlling various lyophilization conditions.

Commonly used protectant include saccharides, polyols, polymers, surfactants, some proteins and amino acids etc. We usually add 8% (mass ratio by volume) of trehalose and mannitol as lyoprotectant. Trehalose can significantly prevent the alter of the protein secondary structure, the extension and aggregation of proteins during freeze-drying process; mannitol is also a universal applied protectant and fillers, which can reduce the aggregation of certain proteins after lyophilization.

Our protein products do not contain carrier protein or other additives (such as bovine serum albumin (BSA), human serum albumin (HSA) and sucrose, etc., and when lyophilized with the solution with the lowest salt content, they often cannot form A white grid structure, but a small amount of protein is deposited in the tube during the freeze-drying process, forming a thin or invisible transparent protein layer.

Reminder: Before opening the tube cap, we recommend that you quickly centrifuge for 20-30 seconds in a small centrifuge, so that the protein attached to the tube cap or the tube wall can be aggregated at the bottom of the tube. Our quality control procedures ensure that each tube contains the correct amount of protein, and although sometimes you can't see the protein powder, the amount of protein in the tube is still very precise.

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