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>   首页   >   产品   >   一抗   >   癌症   >   PFKL Antibody (Center K433)   

PFKL Antibody (Center K433)

Purified Rabbit Polyclonal Antibody (Pab)

     
  • 1 - PFKL Antibody (Center K433) AP8136c
    Anti-PFKL Ctr Antibody at 1:1000 dilution + LNCaP whole cell lysate Lysates/proteins at 20 µg per lane. Secondary Goat Anti-Rabbit IgG, (H+L), Peroxidase conjugated at 1/10000 dilution. Predicted band size : 85 kDa Blocking/Dilution buffer: 5% NFDM/TBST.
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB, E
Primary Accession P17858
Reactivity Human
Host Rabbit
Clonality Polyclonal
Isotype Rabbit IgG
Calculated MW 85018 Da
Antigen Region 371-399 aa
Additional Information
Gene ID 5211
Other Names ATP-dependent 6-phosphofructokinase, liver type {ECO:0000255|HAMAP-Rule:MF_03184}, ATP-PFK {ECO:0000255|HAMAP-Rule:MF_03184}, PFK-L, 27111 {ECO:0000255|HAMAP-Rule:MF_03184}, 6-phosphofructokinase type B, Phosphofructo-1-kinase isozyme B, PFK-B, Phosphohexokinase {ECO:0000255|HAMAP-Rule:MF_03184}, PFKL
Target/Specificity This PFKL antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 371-399 amino acids from the Central region of human PFKL.
Dilution WB~~1:1000
E~~Use at an assay dependent concentration.
Format Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.
StorageMaintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
PrecautionsPFKL Antibody (Center K433) is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name PFKL (HGNC:8876)
Function Catalyzes the phosphorylation of D-fructose 6-phosphate to fructose 1,6-bisphosphate by ATP, the first committing step of glycolysis (PubMed:22923583). Negatively regulates the phagocyte oxidative burst in response to bacterial infection by controlling cellular NADPH biosynthesis and NADPH oxidase-derived reactive oxygen species. Upon macrophage activation, drives the metabolic switch toward glycolysis, thus preventing glucose turnover that produces NADPH via pentose phosphate pathway (By similarity).
Cellular Location Cytoplasm {ECO:0000255|HAMAP-Rule:MF_03184}.
Research Areas

For Research Use Only. Not For Use In Diagnostic Procedures.

BACKGROUND

Phosphofructokinase (PFK), a major regulatory enzyme in all cells of the body, catalyzes the metabolism of sugar, and thereby is pivotal in the production of energy to maintain normal cell function. In human there are three structural loci controlling PFK: M (muscle), L (liver), and P (platelet) type subunits, which are variably expressed in different tissues; human diploid fibroblasts and leukocytes express all three genes. PFK, a tetramer formed by the random association of the products of two separate gene loci to form the five possible tetramers. PFKs of muscle and liver are homotetramers of the M and L subunits, respectively. Red cells have all five isozymes: M4, M3L, M2L2, ML3, and L4. PFK is an allosteric enzyme activated by ADP, AMP, or fructose bisphosphate and inhibited by ATP or citrate. PFK catalyzes the key controlling step of glycolytic pathway. PFK deficiency can present as mild to life-threatening episodic illness. A hallmark sign of this disease is intermittent dark urine, with the color of the urine ranging from orange to dark coffee-brown, which commonly develops following strenuous exercise. The mean red cell PFK is elevated in persons with Down syndrome.

REFERENCES

Strausberg, R.L., et al., Proc. Natl. Acad. Sci. U.S.A. 99(26):16899-16903 (2002).
Hattori, M., et al., Nature 405(6784):311-319 (2000).
Elson, A., et al., Genomics 7(1):47-56 (1990).
Levanon, D., et al., DNA 8(10):733-743 (1989).

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