INSR(Insulin Receptor) Antibody (N-term) 精选
Purified Rabbit Polyclonal Antibody (Pab)
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- 文献引用 : 1
- 实验流程
- 背景知识
Application
| 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 |
| 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. |
| Storage | Maintain 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. |
| Precautions | INSR(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.

Provided below are standard protocols that you may find useful for product applications.
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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