SDF-1α [CXCL12] (human):Fc (human) (rec.)
|Synonyms||CXCL12; C-X-C Motif Chemokine 12; PBSF; SCYB12; TLSF; TPAR1|
|Source/Host||HEK 293 cells|
The extracellular domain of human SDF-1α (aa 22-89) is fused to the N-terminus of the Fc region of human IgG1.
|Endotoxin Content||<5EU/mg protein (LAL test; Lonza).|
Reconstitute 50µg vial in 50µl sterile water.
Add 1X PBS to the desired protein concentration.
|Formulation||Lyophilized from 0.2μm-filtered solution in PBS.|
|Protein Negative Control|
|Other Product Data||
NCBI reference NP_954637.1: SDF-1α (human)
|Declaration||Manufactured by Chimerigen.|
|Shipping and Handling|
|Short Term Storage||+4°C|
|Long Term Storage||-20°C|
Avoid freeze/thaw cycles.
Centrifuge lyophilized vial before opening and reconstitution.
Stable for at least 1 year after receipt when stored at -20°C.
Working aliquots are stable for up to 3 months when stored at -20°C.
|Product Specification Sheet|
The human stromal cell-derived factor-1 (SDF1), also known as CXCL12, is a small (8 kDa) cytokine that belongs to the CXC chemokine subfamily. SDF1 is widely expressed in various organs including heart, liver, brain, kidney, skeletal muscle, and lymphoid organs, and is highly conserved between species. SDF1 is expressed in two isoforms from a single gene that encodes two splice variants, SDF1α and SDF1β, which are identical except for the four residues present in the C-terminus of SDF1β but absent from SDF1α. As a highly efficacious lymphocyte chemoattractant, SDF1 activates and directs the migration of leukocytes in response to proinflammatory stimuli such as LPS, TNF, or interleukins. It has been demonstrated that SDF1 promotes tumor growth and malignancy, enhances tumor angiogenesis, participates in tumor metastasis, and thus plays an important role in carcinoma pathogenesis. In addition, SDF1 is identified as the biological ligand for CXC-chemokine receptor 4 (CXCR4), which is widely expressed in leukocytes and acts as the cofactor for HIV-1 entry, and inhibits the HIV-1 infection. Furthermore, SDF1 is rapidly inactivated via N-terminal processing by cathepsin G associated with the membrane of B-cells, NK cells and to a lesser extent, T-cells.