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AHSP Antibody (Center)

Purified Rabbit Polyclonal Antibody (Pab)

     
  • 1 - AHSP Antibody (Center) AP22199c
    Anti-AHSP Antibody (Center) at 1:1000 dilution + human fetal thymus lysate Lysates/proteins at 20 µg per lane. Secondary Goat Anti-Rabbit IgG, (H+L), Peroxidase conjugated at 1/10000 dilution. Predicted band size : 12 kDa Blocking/Dilution buffer: 5% NFDM/TBST.
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Product info
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 Q9NZD4
Reactivity Human
Host Rabbit
Clonality polyclonal
Isotype Rabbit Ig
Calculated MW 11840 Da
Additional info
Gene ID 51327
Other Names Alpha-hemoglobin-stabilizing protein, Erythroid differentiation-related factor, Erythroid-associated factor, AHSP, EDRF, ERAF
Target/Specificity This AHSP antibody is generated from a rabbit immunized with a KLH conjugated synthetic peptide between 39-73 amino acids from the Central region of human AHSP.
Dilution WB~~1:1000
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.
PrecautionsAHSP Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name AHSP
Synonyms EDRF, ERAF
Function Acts as a chaperone to prevent the harmful aggregation of alpha-hemoglobin during normal erythroid cell development. Specifically protects free alpha-hemoglobin from precipitation. It is predicted to modulate pathological states of alpha-hemoglobin excess such as beta-thalassemia.
Cellular Location Cytoplasm.
Tissue Location Expressed in blood and bone marrow.
Research Areas

BACKGROUND

Acts as a chaperone to prevent the harmful aggregation of alpha-hemoglobin during normal erythroid cell development. Specifically protects free alpha-hemoglobin from precipitation. It is predicted to modulate pathological states of alpha-hemoglobin excess such as beta-thalassemia.

REFERENCES

Miele G.,et al.Nat. Med. 7:361-364(2001).
Zhang Q.-H.,et al.Genome Res. 10:1546-1560(2000).
Michel U.,et al.Submitted (JAN-2002) to the EMBL/GenBank/DDBJ databases.
Finning K.,et al.Submitted (FEB-2002) to the EMBL/GenBank/DDBJ databases.
Kihm A.J.,et al.Nature 417:758-763(2002).

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