Equine TGF-beta 1組換え体(リコンビナント)タンパク質 | Recombinant Equine TGF-beta 1

R&D Systems社製の高品質なEquine TGF-beta 1の組換え体タンパク質(Recombinant Equine TGF-beta 1)です。

※本製品は研究用です。研究用以外には使用できません。

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R&D Systems社組換え体タンパク質製品では通常ウシ血清アルブミン(BSA)をキャリアタンパク質として加えています。キャリアタンパク質を加えることで組換え体タンパク質の安定性が高まり、使用期限が長くなります。また、より濃度の低い溶液での保管も可能となります。CF製品はBSAが含まれない製品となります。一般的に細胞培養や、ELISAのスタンダードにはBSA含有製品を推奨しています。CF製品はBSAが影響してしまうアプリケーションに推奨されます。

TGF-beta 1 (transforming growth factor beta 1) is one of three closely related mammalian members of the large TGF-beta superfamily that share a characteristic cystine knot structure (1-7). TGF-beta 1, -2 and -3 are highly pleiotropic cytokines that are proposed to act as cellular switches that regulate processes such as immune function, proliferation, and epithelial-mesenchymal transition (1-4). Each TGF-beta isoform has some non-redundant functions; for TGF-beta 1, mice with targeted deletion show defects in hematopoiesis and endothelial differentiation and die of overwhelming inflammation (2). Equine TGF-beta 1 cDNA encodes a 390 amino acid (aa) precursor that contains a 29 aa signal peptide and a 361 aa proprotein (8). A furin-like convertase processes the proprotein to generate an N-terminal 249 aa latency-associated peptide (LAP) and a C-terminal 112 aa mature TGF-beta 1 (8, 9). Disulfide-linked homodimers of LAP and TGF-beta 1 remain non-covalently associated after secretion, forming the small latent TGF-beta 1 complex (8-10). Covalent linkage of LAP to one of three latent TGF-beta binding proteins (LTBPs) creates a large latent complex that may interact with the extracellular matrix (9, 10). TGF-beta is activated from latency by pathways that include actions of the protease plasmin, matrix metalloproteases, thrombospondin 1 and a subset of integrins (10). Mature equine TGF-beta 1 shares 98% aa identity with mouse, rat, and human TGF-beta 1, 99% aa identity with pig and dog TGF-beta 1, and 88% aa identity with cow TGF-beta 1. It demonstrates cross-species activity (1). TGF-beta 1 signaling begins with high-affinity binding to a type II Ser/Thr kinase receptor termed TGF-beta RII. This receptor then phosphorylates and activates a second Ser/Thr kinase receptor, TGF-beta RI/ALK-5, or alternatively, ALK-1.This complex phosphorylates and activates Smad proteins that regulate transcription (3, 11, 12). Contributions of the accessory receptors TGF-beta RIII/Betaglycan and Endoglin/CD105, or use of Smad-independent signaling pathways, allow for disparate actions observed in response to TGF-beta in different contexts (11).