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Plectin His Tag Protein, Human

Plectin His Tag Protein, Human

Catalog Number: UA016100 Brand: UA BIOSCIENCE
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$235 USD
$235 USD
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Product Details

Product Specification


Species Human
Synonyms PCN, PLTN, Plectin-1, PLEC1
Accession Q15149-1
Amino Acid Sequence

Ala4377-Ala4684 with His Tag at the N-Terminus
Expression System HEK293
Molecular Weight

40-60kDa (Reducing)
Purity ＞90% by SDS-PAGE
Conjugation Unconjugated
Tag His Tag
Physical Appearance Lyophilized powder
Storage Buffer

PBS, pH7.4, 5% trehalose
Reconstitution

Reconstitute at 0.1-1 mg/ml according to the size in ultrapure water after rapid centrifugation.
Stability & Storage

· 12 months from date of receipt, lyophilized powder stored at -20 to -80℃.
· 3 months, -20 to -80℃ under sterile conditions after reconstitution.
· 1 week, 2 to 8℃ under sterile conditions after reconstitution.
· Please avoid repeated freeze-thaw cycles.
Reference

1.Smith FJ, Eady RA, Leigh IM, McMillan JR, Rugg EL, Kelsell DP, Bryant SP, Spurr NK, Geddes JF, Kirtschig G, Milana G, de Bono AG, Owaribe K, Wiche G, Pulkkinen L, Uitto J, McLean WH, Lane EB. Plectin deficiency results in muscular dystrophy with epidermolysis bullosa. Nat Genet. 1996 Aug;13(4):450-7.
2.McLean WH, Pulkkinen L, Smith FJ, Rugg EL, Lane EB, Bullrich F, Burgeson RE, Amano S, Hudson DL, Owaribe K, McGrath JA, McMillan JR, Eady RA, Leigh IM, Christiano AM, Uitto J. Loss of plectin causes epidermolysis bullosa with muscular dystrophy: cDNA cloning and genomic organization. Genes Dev. 1996 Jul 15;10(14):1724-35. 

Background

Plectin is a large cytolinker protein composed of an N-terminal actin-binding domain, a central rod-shaped α-helical coiled-coil region, and a C-terminal intermediate filament-binding domain, with multiple alternatively spliced isoforms enabling diverse subcellular localization; its functional core lies in bridging microfilaments, intermediate filaments, and microtubule networks to maintain cellular mechanical stability, while also participating in hemidesmosome assembly, myofibril integrity maintenance, and signal transduction regulation. Clinically, PLEC gene mutations cause epidermolysis bullosa simplex (EBS) and its variant subtypes with muscular dystrophy, pyloric atresia, or cardiomyopathy, collectively termed "plectinopathies," with pathological mechanisms involving dermal-epidermal junction disruption, desmin aggregation in muscle fibers, and mitochondrial dysfunction, while recent therapeutic strategies such as chemical chaperone approaches have provided new directions for treatment.

Picture

SDS-PAGE

1μg (R: reducing condition).