Product name: Thymosin β4
Synonyms: Tβ4,thymosin beta4,T beta-4,Fx,Fx Peptide, Thymosin Beta 4, Ac-SDKPDMAEIEKFDKSKLKKTETQEKNPLPSKETIEQEKQAGES,
CAS NO.: 77591-33-4
Modifications: N-terminal acetylation,
Counter ion: Trifluoacetate
Format: Lyophilized powder
Description: Thymosin β4 (Tβ4) is a highly conserved peptide with immunomodulatory properties. Migration is an important process in development, repair, and certain pathologies. Migration is also important in the process of angiogenesis, and Tβ4 has been shown to promote angiogenesis in many tissue sites, with the exception of the cornea. It promotes dermal and ocular repair in part due to its potent chemotactic activity associated with the rapid entry of cells into the wound . It also promotes the migration of various other cells, including stem cells from the bulge region of hair follicles, resulting in increased hair growth; tumor cells, resulting in increased metastasis; and embryonic progenitor cells from cardiac tissue, resulting in the formation of new vessels. Tβ4 up-regulates metalloproteinase activity, which is important in cell migration, tissue repair, and tumor metastasis. It promotes NK cell engulfment and stablin-2-mediated cytotoxicity, which are important in repair processes. Likewise, the antiapoptotic activity of Tβ4 results in cell survival after injury, and thus affects repair by an additional mechanism, i.e., preventing cell loss . The ability of Tβ4 to block apoptosis and down-regulate inflammatory cytokines may explain its antiinflammatory activity. In vitro, down-regulation of Tβ4 with a gene-silencing approach decreases cell survival and increases hypoxia-induced apoptosis. Tβ4 also increases oxidative enzymes and protects cells and tissues from oxidative damage . In the case of peroxide damage, it reduces caspase 9 activation and intracellular ROS (reactive oxygen species) levels, and thus increases cell viability. The expression of manganese superoxide dismutases (SOD) and copper/zinc SOD increased along with increased catalase, thereby providing better protection from cell damage and better survival. Tβ4 is reduced in both human and animal blood after LPS administration and during septic shock, and its administration to animals treated with LPS significantly reduces lethality and inflammatory mediators in endotoxin-induced septic shock. Most recently, increased apoptosis in patients with septic shock and in animals receiving LPS was shown to play a key role in the high mortality observed, suggesting a potential therapeutic role for Tβ4 in sepsis or other types of widespread injury such as large burns.
Uniprot ID: P62328
Usage: For Scientific Research Use Only, Not for Human Use.