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Description
PFKL+PFKM Recombinant Rabbit mAb (S-1302-31)Product Specification Host Rabbit Antigen PFKL+PFKM Synonyms ATP dependent 6 phosphofructokinase, liver type; ATP PFK; PFK L; 6 phosphofructokinase type B; Phosphofructo 1 kinase isozyme B (PFK B); Phosphohexokinase; ATP dependent 6 phosphofructokinase, muscle type; PFK M; 6 phosphofructokinase type A; Phosphofructo 1 kinase isozyme A (PFK A); Phosphohexokinase; PFKX Immunogen Synthetic Peptide Location Cytoplasm Accession P17858 P08237 Clone Number S
Product Specification
| Host | Rabbit |
| Antigen | PFKL+PFKM |
| Synonyms | ATP-dependent 6-phosphofructokinase, liver type; ATP-PFK; PFK-L; 6-phosphofructokinase type B; Phosphofructo-1-kinase isozyme B (PFK-B); Phosphohexokinase; ATP-dependent 6-phosphofructokinase, muscle type; PFK-M; 6-phosphofructokinase type A; Phosphofructo-1-kinase isozyme A (PFK-A); Phosphohexokinase; PFKX |
| Immunogen | Synthetic Peptide |
| Location | Cytoplasm |
| Accession | P17858、 P08237 |
| Clone Number | S-1302-31 |
| Antibody Type | Recombinant mAb |
| Isotype | IgG |
| Application | WB, IHC-P, ICC |
| Reactivity | Hu, Ms, Rt |
| Positive Sample | HeLa, A431, SK-BR-3, HCT 116, RAW264.7, NIH/3T3, C6, PC-12 |
| Purification | Protein A |
| Concentration | 0.5 mg/ml |
| Conjugation | Unconjugated |
| Physical Appearance | Liquid |
| Storage Buffer | PBS, 40% Glycerol, 0.05% BSA, 0.03% Proclin 300 |
| Stability & Storage | 12 months from date of receipt / reconstitution, -20 °C as supplied |
Dilution
| application | dilution | species |
| WB | 1:1000-1:2000 | Hu, Ms, Rt |
| IHC-P | 1:2000 | Hu, Ms, Rt |
| ICC | 1:500 | Hu |
Background
PFKL and PFKM are tissue-specific isoforms of phosphofructokinase-1 (PFK-1) that catalyze the committed step of glycolysis by phosphorylating fructose-6-phosphate to fructose-1,6-bisphosphate; PFKL (≈83 kDa) forms homotetrameric L4 complexes most abundant in liver, whereas PFKM (≈85 kDa) forms homotetrameric M4 complexes predominant in muscle, yet both can co-assemble into heterotetramers (e.g., M3L, M2L2, ML3) in cells such as erythrocytes, enabling finely tuned allosteric regulation by metabolites (activated by ADP, AMP, fructose-2,6-bisphosphate; inhibited by ATP, citrate) and post-translational modifications (phosphorylation, GlcNAcylation, S-nitrosylation, ubiquitination) that integrate nutritional and energy stress signals to control glucose flux, NADPH balance, and downstream biosynthetic pathways critical for systemic glucose homeostasis, redox buffering, and cancer metabolic reprogramming.
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