pro-TGF-beta 1

• Species: Homo sapiens, human
• Tags: His-Tag, N-terminal
• Sequence without tags (AA 30-390):
  MELVKRKRIEAIRGQILSKLRLASPPSQGEVPPGP
  LPEAVLALYNSTRDRVAGESAEPEPEPEADYYAKEVTRVLMVETHNEIYDKFKQSTHSI
  YMFFNTSELREAVPEPVLLSRAELRLLRLKLKVEQHVELYQKYSNNSWRYLSNRLLAPSD
  SPEWLSFDVTGVVRQWLSRGGEIEGFRLSAHCSCDSRDNTLQVDINGFTTGRRGDLATIH
  GMNRPFLLLMATPLERAQHLQSSRHRRALDTNYCFSSTEKNCCVRQLYIDFRKDLGWKWI
  HEPKGYHANFCLGPCPYIWSLDTQYSKVLALYNQHNPGASAAPCCVPQALEPLPIVYYVG
  RKPKVEQLSNMIVRSCKCS
  

• Expression Host: human, HEK293
• Formulation: PBS; pH 7.4.
• Format: Liquid, stored and shipped at -80°C
• Purity: > 95% as determined by SDS-PAGE

Transforming growth factor beta 1 (TGF-β1) belongs to the transforming growth factor beta superfamily of cytokines and is involved in a myriad of cellular functions including the control of cell growth, cell proliferation, cell differentiation, and apoptosis.
The transforming growth factor beta-1 is synthesized as precursor consisting of the latency-associated peptide (LAP, 249 aa) and the transforming growth factor beta 1 (112 aa). The precursor is also named small latent complex (SLC) or latent TGF-ß1. The precursor proprotein is cleaved in the Golgi apparatus by Furin, but the disulfide-linked homodimers of LAP and TGF-beta 1 remain non‑covalently associated after secretion.
TGF-ß1 activation from latency is controlled both spatially and temporally, by multiple pathways that include actions of proteases such as plasmin and MMP9, and/or by thrombospondin 1 or selected integrins. Once activated following release of LAP, TGF-beta-1 acts by binding to TGF-beta receptors (TGFBR1 and TGFBR2), which transduce signals.

Mutations within the LAP are associated with Camurati-Engelmann disease, a rare sclerosing bone dysplasia characterized by inappropriate presence of active TGF-beta 1.

SDS-PAGE/Coll. Coomassie	Histogram of marked lane in gel picture

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