|Positive WB detected in||A431 cells, HepG2 cells, HEK-293 cells, HeLa cells, PC-12 cells, PC-3 cells, NIH/3T3 cells, mouse liver tissue, rat liver tissue|
|Positive IP detected in||SW 1990 cells|
|Western Blot (WB)||WB : 1:5000-1:50000|
|Immunoprecipitation (IP)||IP : 0.5-4.0 ug for IP and 1:1000-1:4000 for WB|
|Sample-dependent, check data in validation data gallery|
17811-1-AP targets PGK1 in WB, IP, IHC, IF, ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||human, mouse|
|Host / Isotype||Rabbit / IgG|
|Immunogen||PGK1 fusion protein Ag12119|
|Full Name||phosphoglycerate kinase 1|
|Calculated molecular weight||417 aa, 45 kDa|
|Observed molecular weight||40-45 kDa|
|GenBank accession number||BC103752|
|Gene ID (NCBI)||5230|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage. 20ul sizes contain 0.1% BSA.|
The PGK1 gene encodes phosphoglycerate kinase-1, also known as ATP:3-phosphoglycerate 1-phosphotransferase (EC 126.96.36.199), which catalyzes the reversible conversion of 1,3-diphosphoglycerate to 3-phosphoglycerate during glycolysis, generating one molecule of ATP. It Belongs to the phosphoglycerate kinase family and defects in PGK1 are the cause of phosphoglycerate kinase 1 deficiency (PGK1D). PGK1 has 2 isoforms with the molecular mass of 45 kDa and 41 kDa.
Transcriptional Regulation of the Warburg Effect in Cancer by SIX1.
A glycolytic shift in Schwann cells supports injured axons.
The long noncoding RNA glycoLINC assembles a lower glycolytic metabolon to promote glycolysis.
Low chorionic villous succinate accumulation associates with recurrent spontaneous abortion risk.
Fasting inhibits aerobic glycolysis and proliferation in colorectal cancer via the Fdft1-mediated AKT/mTOR/HIF1α pathway suppression.
Inhibition of PGK1 attenuates autoimmune myocarditis by reprogramming CD4+ T cells metabolism