growth-regulated α protein

Growth-regulated alpha protein (CXCL1,KC), is a member of the alpha chemokine subfamily, was initially identified as an immediate early gene induced in mouse fibroblasts by platelet-derived growth factor. The N-terminal processed form KC(5-72) of the protein is produced by proteolytic cleavage after secretion from bone marrow stromal cells, and shows a highly enhanced hematopoietic activity. Mouse KC shows approximately 63% identity to that of mouse MIP-2. KC is also approximately 60% identical to the human GROs. It has been suggested that mouse KC and MIP-2 are the orthologs of the human GROs and rat CINCs. Cxcl1 has chemotactic activity for neutrophils, and contributes to neutrophil activation during inflammation. Hematoregulatory chemokine, in vitro, suppresses hematopoietic progenitor cell proliferation.

Expression system: E. coli
Length: 35-107, Full Length of Mature Protein
Activity: Cell Activity

Expression system: E. coli
Length: 25-96, Full Length of Mature Protein
Activity: Cell Activity

Expression system: E. coli
Length: 28-100, Full Length of Mature Protein
Activity: Not Tested

CXCL1 Protein, Mouse, Recombinant (CHO) is expressed in CHO Cells. The accession number is P12850.

Biliverdin reductase (hBVR) is a serine threonine kinase that catalyzes reduction of the heme oxygenase (HO) activity product, biliverdin, to bilirubin. BVR consists of an N-terminal dinucleotide-binding domain (Rossmann-fold) and a C-terminal domain that contains a six-stranded β-sheet that is flanked on one face by several α-helices. The C-terminal and N-terminal domains interact extensively, forming the active site cleft at their interface. Biliverdin reductase (BVR) catalyzes the last step in heme degradation by reducing the γ-methene bridge of the open tetrapyrrole, biliverdin IXα, to bilirubin with the concomitant oxidation of a β-nicotinamide adenine dinucleotide (NADH) or β-nicotinamide adenine dinucleotide phosphate (NADPH) cofactor. It is now recognized that human BVR (hBVR) is a dual-specificity kinase (Ser Thr and Tyr) upstream activator of the insulin insulin growth factor-1 (IGF-1) and mitogen-activated protein kinase (MAPK) signaling pathways. Human BVR (hBVR) is essential for MAPK-extracellular signal-regulated kinase (ERK)1 2 (MEK)-eukaryotic-like protein kinase (Elk) signaling and has been identified as the cytoplasm-nuclear heme transporter of ERK1 2 and hematin, the key components of stress-responsive gene expression.