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Human Recombinant PLGF-3 (from E. coli)

Dodavatel: Shenandoah Biotechnology

Popis: Placenta growth factor (PlGF) is a member of the vascular endothelial growth factor (VEGF) family and promotes endothelial cell growth and angiogenesis. PlGF is secreted as a homodimer and may also form a heterodimer with VEGF. PlGF is detected in the placenta, heart, lungs, thyroid, and adipose tissues. Circulating PlGF levels are correlated with colorectal and renal cancers, as well as atherosclerosis and ischemic heart disease. There are four alternatively spliced PlGF isoforms (PlGF-1, PlGF-2, PlGF-3, and PlGF-4), each with unique secretion patterns and heparin-binding affinities. PlGF-3 lacks a heparin-binding domain and signals through the VEGFR-1 receptor.

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Human Recombinant DFF45 (from E. coli)

Katalogové číslo: (PRSI92-051)

Dodavatel: ProSci Inc.

Popis: DNA Fragmentation Factor Subunit Alpha (DFFA). DFFA exists as a heterodimer (DFF) with DFFB. DFF is activated once DFFA is cleaved by Caspase-3. The cleaved fragments of DFFA detach from DFFB (the active component of DFF), which in turn triggers DNA fragmentation as well as chromatin condensation during apoptosis. A reduced level of DFFA detected in ovarian endometriosis may be a part of an apoptosis-resistant mechanism enhancing the disease progression.

Měrná jednotka: 1 * 0,05 mg

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Human Recombinant BID (from E. coli)

Katalogové číslo: (PRSI91-089)

Dodavatel: ProSci Inc.

Popis: BH3-Interacting Domain Death Agonist (BID) is a member of the Bcl-2 protein family which regulates outer mitochondrial membrane permeability. BID is a pro-apoptotic member that causes cytochrome c to be released from the mitochondria intermembrane space into the cytosol. Interaction of Bid with Bak causes altered mitochondrial membrane permeability. BID contains only the BH3 domain, which is required for its interaction with the Bcl-2 family proteins and for its pro-death activity. BID is susceptible to proteolytic cleavage by caspases, calpains, Granzyme B and cathepsins. It is an integrating key regulator of the intrinsic death pathway that amplifies caspase-dependent and caspase-independent execution of neuronal apoptosis. Therefore pharmacological inhibition of BID provides a promising therapeutic strategy in neurological diseases where programmed cell death is prominent, and also offer a new strategy for the treatment of acute renal failure associated with ischemia-reperfusion. BID receives direct inputs from a key regulator of the cell cycle arrest/DNA repair machinery (ATM), and therefore is an excellent candidate to coordinate genotoxic stress responses and apoptotic cell death. BID is a novel pro-apoptosis Bcl-2 family protein that is activated by caspase 8 in response to Fas/TNF-R1 death receptor signals. Deletion of BID inhibits carcinogenesis in the liver, although this genetic alteration promotes tumorigenesis in the myeloid cells. This is likely related to the function of BID to promote cell cycle progression into S phase. BID could be also involved in the maintenance of genomic stability by engaging at mitosis checkpoint.

Měrná jednotka: 1 * 0,05 mg

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