Anti-phospho-IR (Tyr1322), clone 21G12

Species Reactivity	Key Applications	Host	Format	Antibody Type
Ca, H, M	ELISA, WB	M	Purified	Monoclonal Antibody

Species Reactivity

Key Applications

Host

Format

Antibody Type

Ca, H, M

ELISA, WB

Purified

Monoclonal Antibody

Description
Catalogue Number	04-300
Brand Family	Upstate
Trade Name	Upstate
Description	Anti-phospho-Insulin Receptor (Tyr 1322) Antibody, clone 21G12
Alternate Names	INSR

Description

Catalogue Number

04-300

Brand Family

Upstate

Trade Name

Upstate

Description

Anti-phospho-Insulin Receptor (Tyr 1322) Antibody, clone 21G12

Alternate Names

INSR

Product Information
Format	Purified
Control	Includes pervanadate treated HEK293 lysate as a positive control.
Presentation	Lyophilized in 2X PBS containing 0.09% sodium azide, PEG, and sucrose.

Product Information

Format

Purified

Control

Includes pervanadate treated HEK293 lysate as a positive control.

Presentation

Lyophilized in 2X PBS containing 0.09% sodium azide, PEG, and sucrose.

Applications
Application	Anti-phospho-Insulin Receptor Antibody, clone 21G12 is an antibody against phospho-Insulin Receptor (Tyr 1322) for use in ELISA & WB.
Key Applications	ELISA Western Blotting

Applications

Application

Anti-phospho-Insulin Receptor Antibody, clone 21G12 is an antibody against phospho-Insulin Receptor (Tyr 1322) for use in ELISA & WB.

Key Applications

ELISA
Western Blotting

Biological Information
Immunogen	KLH-conjugated synthetic peptide encompassing the surrounding amino acids of Tyrosine 1322 on phosphorylated insulin receptor
Clone	21g12
Host	Mouse
Specificity	Recognizes phosphorylated domain of Insulin receptor on Tyrosine 1322.
Isotype	IgG1
Species Reactivity	Canine Human Mouse
Antibody Type	Monoclonal 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 IR HHF5
Modifications	Phosphorylation
Purification Method	Subsequent thiophilic adsorption and size exclusion chromatography
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	97 kDa

Biological Information

Immunogen

KLH-conjugated synthetic peptide encompassing the surrounding amino acids of Tyrosine 1322 on phosphorylated insulin receptor

Clone

21g12

Host

Mouse

Specificity

Recognizes phosphorylated domain of Insulin receptor on Tyrosine 1322.

Isotype

IgG1

Species Reactivity

Canine
Human
Mouse

Antibody Type

Monoclonal 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
IR
HHF5

Modifications

Phosphorylation

Purification Method

Subsequent thiophilic adsorption and size exclusion chromatography

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

97 kDa

Product Usage Statements
Quality Assurance	Routinely evaluated by immunoblot.
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

Quality Assurance

Routinely evaluated by immunoblot.

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	2 years at -20°C from date of shipment. Reconstitute prior to use. Reconstitute with 1 mL H₂O for 15 min at room temperature. Reconstituted aliquots should be stored frozen at -80°C. Thawed aliquots may be stored at 4°C for up to 3 months. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance.

Storage and Shipping Information

Storage Conditions

2 years at -20°C from date of shipment. Reconstitute prior to use. Reconstitute with 1 mL H₂O for 15 min at room temperature. Reconstituted aliquots should be stored frozen at -80°C. Thawed aliquots may be stored at 4°C for up to 3 months. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance.

Packaging Information
Material Size	100 µg

Packaging Information

Material Size

100 µg

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 (Tyr1322), clone 21G12

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