SIL1 (SIL1 nucleotide exchange factor) is a glycoprotein present in the membrane of endoplasmic reticulum. It is composed of an N-terminal endoplasmic reticulum (ER) target zone, four armadillo repeats (ARMs), two N-linked glycosylation sites and a C-terminal putative ER retention tetrapeptide. It is expressed in the pancreatic ß cells and helps in several activities including islet insulin content, islet sizing, glucose tolerance, and glucose-stimulated insulin secretion in vivo.
Synonyms: Anti-BAP; Anti-BiP-associated protein; Anti-Nucleotide exchange factor SIL1 precursor
Storage: -20C
Application: All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project (www.proteinatlas.org)and as a result, are supported by the most extensive characterization in the industry. The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. To view these protocols and other useful information about Prestige Antibodies and the HPA, visit sigma.com/prestige.
Biochem Physiol Actions: SIL1 (SIL1 nucleotide exchange factor) is involved in ß cell function. During protein folding, it binds to HSP (heat shock protein) to acts as an adenine nucleotide exchange factor. It binds to the ADP-bound HSPA5, which further facilitates ADP release as well as the release of HSPA5 from its substrates. As a result, ATP is attached with the HSPA5. Thus, SIL1 stabilizes proper folding of newly synthesized proteins and degrades those proteins that fail to mature properly. Mutations in SIL1 cause cerebellar ataxia, chronic myopathy, cataracts, delayed motor development and intellectual disability, collectively known as Marinesco-Sjögren syndrome.
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