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NME3 Antibody (Center) 精选

Purified Rabbit Polyclonal Antibody (Pab)

     
  • 1 - NME3 Antibody (Center) AP7156a
    Western blot analysis of anti-NME3 Pab (Cat. #AP7156a) in CEM cell line tissue lysate (35ug/lane).NME3(arrow) was detected using the purified Pab.
  • 14 - NME3 Antibody (Center) AP7156a
    Formalin-fixed and paraffin-embedded human cancer tissue reacted with the primary antibody, which was peroxidase-conjugated to the secondary antibody, followed by DAB staining. This data demonstrates the use of this antibody for immunohistochemistry; clinical relevance has not been evaluated. BC = breast carcinoma; HC = hepatocarcinoma.
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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, IHC-P, E
Primary Accession Q13232
Reactivity Mouse, Human
Predicted Rat, Bovine
Host Rabbit
Clonality Polyclonal
Isotype Rabbit IgG
Calculated MW 19015 Da
Antigen Region 51-81 aa
Additional Information
Gene ID 4832
Other Names Nucleoside diphosphate kinase 3, NDK 3, NDP kinase 3, DR-nm23, Nucleoside diphosphate kinase C, NDPKC, nm23-H3, NME3
Target/Specificity This NME3 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 51-81 amino acids from the Central region of human NME3.
Dilution WB~~1:1000
IHC-P~~1:100~500
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.
PrecautionsNME3 Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures.

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

Protein Information
Name NME3 (HGNC:7851)
Function Catalyzes the transfer of a gamma-phosphoryl group from a nucleoside triphosphate, mainly ATP, to a nucleoside diphosphate via a ping-pong mechanism involving a phosphohistidine intermediate, therefore contributing to the nucleoside triphosphate homeostasis (PubMed:11277919, PubMed:30587587, PubMed:39337255). In vitro, can also use other phosphate donors such as UTP and GTP (PubMed:30587587, PubMed:39337255). Independently of its nucleoside diphosphate kinase activity, involved in mitochondrial membrane tethering, a prerequisite for fusion through direct membrane-binding and hexamerization (PubMed:30587587, PubMed:37584589). Involved in DNA repair of both single- and double-stranded breaks by associating with the ribonucleotide reductase (RNR) complex via interaction with the histone acetyltransferase KAT5, facilitating recruitment to DNA damage sites independently of its kinase activity (PubMed:26945015). Inhibits granulocyte differentiation (PubMed:7638209). May be required for ciliary function during renal development (By similarity).
Cellular Location Mitochondrion outer membrane; Peripheral membrane protein. Cytoplasm Cytoplasm, cytoskeleton, cilium basal body {ECO:0000250|UniProtKB:Q9WV85}
Research Areas

BACKGROUND

NME3 mRNA is preferentially expressed at early stages of myeloid differentiation of highly purified CD34(+) cells. Its constitutive expression in a myeloid precursor line, which is growth-factor dependent for both proliferation and differentiation, results in inhibition of granulocytic differentiation induced by granulocyte colony-stimulating factor and causes apoptotic cell death. These results appear consistent with a role for the NME3 gene in normal hematopoiesis and raise the possibility that its overexpression contributes to differentiation arrest, a feature of blastic transformation in chronic myelogenous leukemia.

REFERENCES

Negroni, A., et al., Cell Death Differ. 7(9):843-850 (2000).
Martinez, R., et al., Cancer Res. 57(6):1180-1187 (1997).
Venturelli, D., et al., Proc. Natl. Acad. Sci. U.S.A. 92(16):7435-7439 (1995).

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