Anti-phospho-IR (Tyr972)

Species Reactivity	Key Applications	Host	Format	Antibody Type
H, M	WB	Rb	Affinity Purified	Polyclonal Antibody

Species Reactivity

Key Applications

Host

Format

Antibody Type

H, M

Affinity Purified

Polyclonal Antibody

Description
Catalogue Number	07-838
Brand Family	Upstate
Trade Name	Upstate
Description	Anti-phospho-IR (Tyr972) Antibody
Alternate Names	Insulin Receptor CD220

Description

Catalogue Number

07-838

Brand Family

Upstate

Trade Name

Upstate

Description

Anti-phospho-IR (Tyr972) Antibody

Alternate Names

Insulin Receptor
CD220

Product Information
Format	Affinity Purified
Presentation	100 μL of affinity purified rabbit polyclonal IgG in 50% storage buffer (PBS (without Mg²⁺ and Ca²⁺), pH 7.3 containing 1.0 mg/mL BSA (IgG and protease free) and 0.05% sodium azide) and 50% glycerol.

Product Information

Format

Affinity Purified

Presentation

100 μL of affinity purified rabbit polyclonal IgG in 50% storage buffer (PBS (without Mg²⁺ and Ca²⁺), pH 7.3 containing 1.0 mg/mL BSA (IgG and protease free) and 0.05% sodium azide) and 50% glycerol.

Applications
Application	Anti-phospho-IR (Tyr972) Antibody detects level of phospho-IR (Tyr972) & has been published & validated for use in WB.
Key Applications	Western Blotting

Applications

Application

Anti-phospho-IR (Tyr972) Antibody detects level of phospho-IR (Tyr972) & has been published & validated for use in WB.

Key Applications

Western Blotting

Biological Information
Immunogen	A linear peptide corresponding to amino acid region encompassing the human, mouse and rat phospho-IR (pTyr972).
Host	Rabbit
Specificity	Recognizes phospho-IR (β-subunit) (pTyr972).
Isotype	IgG
Species Reactivity	Human Mouse
Species Reactivity Note	Predicted to cross-react with rat based on sequence homology (100%), but have not been tested.
Antibody Type	Polyclonal Antibody
Entrez Gene Number	NM_000208.2 NM_001079817.1
Entrez Gene Summary	After removal of the precursor signal peptide, the insulin receptor precursor is post-translationally cleaved into two chains (alpha and beta) that are covalently linked. Binding of insulin to the insulin receptor (INSR) stimulates glucose uptake. Two transcript variants encoding different isoforms have been found for this gene.
Gene Symbol	INSR CD220 HHF5 IR
Modifications	Phosphorylation
Purification Method	Affinity Purfied
UniProt Number	P06213
UniProt Summary	FUNCTION: SwissProt: P06213 # This receptor binds insulin and has a tyrosine-protein kinase activity. Isoform Short has a higher affinity for insulin. Mediates the metabolic functions of insulin. Binding to insulin stimulates association of the receptor with downstream mediators including IRS1 and phosphatidylinositol 3'-kinase (PI3K). Can activate PI3K either directly by binding to the p85 regulatory subunit, or indirectly via IRS1. SIZE: 1382 amino acids; 156307 Da SUBUNIT: 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. Interacts with SORBS1 but dissociates from it following insulin stimulation. Binds SH2B2. Interacts with the PTB/PID domains of IRS1 and SHC1 in vitro when autophosphorylated on tyrosine residues. The sequences surrounding the phosphorylated NPXY motif contribute differentially to either IRS1 or SHC1 recognition. Interacts with the SH2 domains of the 85 kDa regulatory subunit of PI3K (PIK3R1) in vitro, when autophosphorylated on tyrosine residues. Interacts with SOCS7. SUBCELLULAR LOCATION: Membrane; Single-pass type I membrane protein. TISSUE SPECIFICITY: Isoform Long and isoform Short are expressed in the peripheral nerve, kidney, liver, striated muscle, fibroblasts and skin. Isoform Short is expressed also in the spleen and lymphoblasts. PTM: 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. & Autophosphorylated on tyrosine residues in response to insulin. & Phosphorylation of Tyr-999 is required for IRS1- and SHC1- binding. DISEASE: SwissProt: P06213 # Defects in INSR are the cause of insulin resistance (Ins resistance) [MIM:125853]. & Defects in INSR are the cause of Rabson-Mendenhall syndrome [MIM:262190]; 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 [MIM:246200]; 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 (NIDDM) [MIM:125853]; also known as diabetes mellitus type 2. & Defects in INSR are the cause of familial hyperinsulinemic hypoglycemia 5 (HHF5) [MIM:609968]. Familial hyperinsulinemic hypoglycemia [MIM:256450], also referred to as congenital hyperinsulinism, nesidioblastosis, or persistent hyperinsulinemic hypoglycemia of infancy (PPHI), is the most common cause of persistent hypoglycemia in infancy and is due to defective negative feedback regulation of insulin secretion by low glucose levels. & Defects in INSR are the cause of insulin-resistant diabetes mellitus with acanthosis nigricans type A (IRAN type A) [MIM:610549]. This syndrome is characterized by the association of severe insulin resistance (manifested by marked hyperinsulinemia and a failure to respond to exogenous insulin) with the skin lesion acanthosis nigricans and ovarian hyperandrogenism in adolescent female subjects. Women frequently present with hirsutism, acne, amenorrhea or oligomenorrhea, and virilization. This syndrome is different from the type B that has been demonstrated to be secondary to the presence of circulating autoantibodies against the insulin receptor. SIMILARITY: SwissProt: P06213 ## Belongs to the protein kinase superfamily. Tyr protein kinase family. Insulin receptor subfamily. & Contains 2 fibronectin type-III domains. & Contains 1 protein kinase domain.
Molecular Weight	155 kDa

Biological Information

Immunogen

A linear peptide corresponding to amino acid region encompassing the human, mouse and rat phospho-IR (pTyr972).

Host

Rabbit

Specificity

Recognizes phospho-IR (β-subunit) (pTyr972).

Isotype

IgG

Species Reactivity

Human
Mouse

Species Reactivity Note

Predicted to cross-react with rat based on sequence homology (100%), but have not been tested.

Antibody Type

Polyclonal Antibody

Entrez Gene Number

Entrez Gene Summary

After removal of the precursor signal peptide, the insulin receptor precursor is post-translationally cleaved into two chains (alpha and beta) that are covalently linked. Binding of insulin to the insulin receptor (INSR) stimulates glucose uptake. Two transcript variants encoding different isoforms have been found for this gene.

Gene Symbol

INSR
CD220
HHF5
IR

Modifications

Phosphorylation

Purification Method

Affinity Purfied

UniProt Number

P06213

UniProt Summary

FUNCTION: SwissProt: P06213 # This receptor binds insulin and has a tyrosine-protein kinase activity. Isoform Short has a higher affinity for insulin. Mediates the metabolic functions of insulin. Binding to insulin stimulates association of the receptor with downstream mediators including IRS1 and phosphatidylinositol 3'-kinase (PI3K). Can activate PI3K either directly by binding to the p85 regulatory subunit, or indirectly via IRS1.
SIZE: 1382 amino acids; 156307 Da
SUBUNIT: 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. Interacts with SORBS1 but dissociates from it following insulin stimulation. Binds SH2B2. Interacts with the PTB/PID domains of IRS1 and SHC1 in vitro when autophosphorylated on tyrosine residues. The sequences surrounding the phosphorylated NPXY motif contribute differentially to either IRS1 or SHC1 recognition. Interacts with the SH2 domains of the 85 kDa regulatory subunit of PI3K (PIK3R1) in vitro, when autophosphorylated on tyrosine residues. Interacts with SOCS7.
SUBCELLULAR LOCATION: Membrane; Single-pass type I membrane protein.
TISSUE SPECIFICITY: Isoform Long and isoform Short are expressed in the peripheral nerve, kidney, liver, striated muscle, fibroblasts and skin. Isoform Short is expressed also in the spleen and lymphoblasts.
PTM: 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. & Autophosphorylated on tyrosine residues in response to insulin. & Phosphorylation of Tyr-999 is required for IRS1- and SHC1- binding.
DISEASE: SwissProt: P06213 # Defects in INSR are the cause of insulin resistance (Ins resistance) [MIM:125853]. & Defects in INSR are the cause of Rabson-Mendenhall syndrome [MIM:262190]; 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 [MIM:246200]; 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 (NIDDM) [MIM:125853]; also known as diabetes mellitus type 2. & Defects in INSR are the cause of familial hyperinsulinemic hypoglycemia 5 (HHF5) [MIM:609968]. Familial hyperinsulinemic hypoglycemia [MIM:256450], also referred to as congenital hyperinsulinism, nesidioblastosis, or persistent hyperinsulinemic hypoglycemia of infancy (PPHI), is the most common cause of persistent hypoglycemia in infancy and is due to defective negative feedback regulation of insulin secretion by low glucose levels. & Defects in INSR are the cause of insulin-resistant diabetes mellitus with acanthosis nigricans type A (IRAN type A) [MIM:610549]. This syndrome is characterized by the association of severe insulin resistance (manifested by marked hyperinsulinemia and a failure to respond to exogenous insulin) with the skin lesion acanthosis nigricans and ovarian hyperandrogenism in adolescent female subjects. Women frequently present with hirsutism, acne, amenorrhea or oligomenorrhea, and virilization. This syndrome is different from the type B that has been demonstrated to be secondary to the presence of circulating autoantibodies against the insulin receptor.
SIMILARITY: SwissProt: P06213 ## Belongs to the protein kinase superfamily. Tyr protein kinase family. Insulin receptor subfamily. & Contains 2 fibronectin type-III domains. & Contains 1 protein kinase domain.

Molecular Weight

155 kDa

Product Usage Statements
Usage Statement	Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

Product Usage Statements

Usage Statement

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

Storage and Shipping Information
Storage Conditions	Stable for 2 years at -20°C from date of shipment. Handling Recommendations: Upon first thaw, and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance. Note: Variability in freezer temperatures below -20°C may cause glycerolcontaining solutions to become frozen during storage.

Storage and Shipping Information

Storage Conditions

Stable for 2 years at -20°C from date of shipment.
Handling Recommendations: Upon first thaw, and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance. Note: Variability in freezer temperatures below -20°C may cause glycerolcontaining solutions to become frozen during storage.

Packaging Information
Material Size	100 µL

Packaging Information

Material Size

100 µL

实验耗材

分子生物学试剂

蛋白与免疫学

生化试剂

细胞及检测试剂

色谱及层析

仪器设备

实验服务

办公用品

Anti-phospho-IR (Tyr972)

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