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>   首页   >   产品   >   一抗   >   癌症   >   INSR(Insulin Receptor) Antibody (N-term)   

INSR(Insulin Receptor) Antibody (N-term) 精选

Purified Rabbit Polyclonal Antibody (Pab)

     
  • 59 - INSR(Insulin Receptor) Antibody (N-term) AP7653A
    Immunohistochemical analysis of paraffin-embedded Human kidney tissue using AP7653A performed on the Leica® BOND RXm. Tissue was fixed with formaldehyde at room temperature, antigen retrieval was by heat mediation with a EDTA buffer (pH9. 0). Samples were incubated with primary antibody(1:500) for 1 hours at room temperature. A undiluted biotinylated CRF Anti-Polyvalent HRP Polymer antibody was used as the secondary antibody.
  • 1 - INSR(Insulin Receptor) Antibody (N-term) AP7653A
    Anti-INSR(Insulin Receptor) Antibody (N-term) at 1:1000 dilution + Mouse liver lysate Lysates/proteins at 20 µg per lane. Secondary Goat Anti-Rabbit IgG, (H+L), Peroxidase conjugated at 1/10000 dilution. Predicted band size : 156 kDa Blocking/Dilution buffer: 5% NFDM/TBST.
  • 1 - INSR(Insulin Receptor) Antibody (N-term) AP7653A
    Western blot analysis of anti-INSR Pab (Cat. #ap7653a) in SKBR-3 cell lysate. INSR (arrow) was detected using purified Pab. Secondary HRP-anti-rabbit was used for signal visualization with chemiluminescence.
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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-Leica, E
Primary Accession P06213
Other Accession P15127, P15208
Reactivity Human, Mouse, Rat
Predicted Mouse, Rat, Bovine, Canine, Rabbit, Chicken
Host Rabbit
Clonality Polyclonal
Isotype Rabbit IgG
Antigen Region 28-57 aa
Additional Information
Other Names Insulin receptor, IR, CD220, Insulin receptor subunit alpha, Insulin receptor subunit beta, INSR
Target/Specificity This INSR(Insulin Receptor) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 28-57 amino acids from the N-terminal region of human INSR(Insulin Receptor).
Dilution WB~~1:1000
IHC-P-Leica~~1:500
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.
PrecautionsINSR(Insulin Receptor) Antibody (N-term) 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
Research Areas

BACKGROUND

INSR is a receptor that binds insulin and has a tyrosine-protein kinase activity. Autophosphorylation activates the kinase activity. This Type I mebrane protein is composed of a tetramer of 2 alpha and 2 beta chains linked by disulfide bonds. The alpha chains contribute to the formation of the ligand-binding domain, while the beta chains carry the kinase domain. After being transported from the endoplasmic reticulum to the Golgi apparatus, the single glycosylated precursor is further glycosylated and then cleaved, followed by its transport to the plasma membrane. Defects in INSR are the cause of insulin resistance of various forms, including mild insulin-resistant diabetes mellitus with acanthosis nigricans, minor physical abnormalities and sometimes polycystic ovaries. Insulin resistance associated with acanthosis nigricans, hirsutism and hyperandrogenism is referred to as insulin resistance type A. Defects in INSR are the cause of Rabson-Mendenhall syndrome, also known as Mendenhall syndrome. It is a severe insulin resistance syndrome characterized by insulin-resistant diabetes mellitus with pineal hyperplasia and somatic abnormalities. Typical features include coarse, senile-appearing facies, dental and skin abnormalities, abdominal distension, and phallic enlargement. Inheritance is autosomal recessive. Defects in INSR are the cause of leprechaunism, also known as Donohue syndrome. Leprechaunism represents the most severe form of insulin resistance syndrome, characterized by intrauterine and postnatal growth retardation and death in early infancy. Inheritance is autosomal recessive. Defects in INSR may be associated with noninsulin-dependent diabetes mellitus.

REFERENCES

George, S., et al., Endocrinology 144(2):631-637 (2003).
Longo, N., et al., Hum. Mol. Genet. 11(12):1465-1475 (2002).
Hamer, I., et al., Diabetologia 45(5):657-667 (2002).
Osawa, H., et al., Clin. Genet. 59(3):194-197 (2001).
Rique, S., et al., Clin. Genet. 57(1):67-69 (2000).

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