Anti-IKKg/IKK3 (mouse monoclonal IgG1)

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

Species Reactivity

Key Applications

Host

Format

Antibody Type

H, M

Purified

Monoclonal Antibody

Description
Catalogue Number	05-631
Brand Family	Upstate
Trade Name	Upstate
Description	Anti-IKKγ Antibody
Overview	IKKγ/IKK3 is also known as NEMO, FIP-3 and IKKAP-1

Description

Catalogue Number

05-631

Brand Family

Upstate

Trade Name

Upstate

Description

Anti-IKKγ Antibody

Overview

IKKγ/IKK3 is also known as NEMO, FIP-3 and IKKAP-1

Product Information
Format	Purified
Presentation	PBS, pH 7.4, containing 0.05% sodium azide

Product Information

Format

Purified

Presentation

PBS, pH 7.4, containing 0.05% sodium azide

Applications
Application	Anti-IKKγ Antibody is an antibody against IKKγ for use in WB.
Key Applications	Western Blotting

Applications

Application

Anti-IKKγ Antibody is an antibody against IKKγ for use in WB.

Key Applications

Western Blotting

Biological Information
Immunogen	His-tagged, full-length human IKKgamma/IKK3
Host	Mouse
Specificity	IKKγ/IKK3
Isotype	IgG
Species Reactivity	Human Mouse
Antibody Type	Monoclonal Antibody
Entrez Gene Number	NM_003639
Entrez Gene Summary	Familial incontinentia pigmenti (IP) is a genodermatosis that segregates as an X-linked dominant disorder and is usually lethal prenatally in males (The International Incontinentia Pigmenti Consortium, 2000 [PubMed 10839543]). In affected females it causes highly variable abnormalities of the skin, hair, nails, teeth, eyes, and central nervous system. The prominent skin signs occur in 4 classic cutaneous stages: perinatal inflammatory vesicles, verrucous patches, a distinctive pattern of hyperpigmentation, and dermal scarring. Cells expressing the mutated X chromosome are eliminated selectively around the time of birth, so females with IP exhibit extremely skewed X-inactivation. Familial incontinentia pigmenti is caused by mutations in the NEMO gene and is here referred to as IP2, or 'classical' incontinentia pigmenti. Sporadic incontinentia pigmenti, the so-called IP1, which maps to Xp11, is categorized as hypomelanosis of Ito (MIM 300337).[supplied by OMIM]
Gene Symbol	IKBKG FIP3 IPD2 NEMO IP2 Fip3p IP1 IKKG IKK-gamma AMCBX1 FIP-3 IKKAP1 IP
Purification Method	Protein G Chromatography
UniProt Number	Q9Y6K9
UniProt Summary	FUNCTION: SwissProt: Q9Y6K9 # Regulatory subunit part of the IKK-signalosome complex activation. Also considered to be a mediator for TAX activation of NF-kappa-B. Could be implicated in NF-kappa-B-mediated protection from cytokine toxicity. SIZE: 419 amino acids; 48198 Da SUBUNIT: Interacts preferentially with IKBKB/IKK-beta but also able to interact with CHUK/IKK-alpha, IKAP, RIP and MAP3K14/NIK. Found in a complex composed of NCOA2, NCOA3, CHUK/IKKA, IKBKB/IKKB and CREBBP. Interacts with COPS3, CYLD, NALP2, TRPC4AP and LRDD. Activated through binding to HTLV-1 Tax oncoprotein. SUBCELLULAR LOCATION: Cytoplasm. Nucleus. TISSUE SPECIFICITY: Heart, brain, placenta, lung, liver, skeletal muscle, kidney and pancreas. DISEASE: SwissProt: Q9Y6K9 # Defects in IKBKG are the cause of X-linked anhidrotic ectodermal dysplasia with immunodeficiency (XL-EDA-ID) [MIM:300291]; also known as hypohidrotic ectodermal dysplasia with immunodeficiency (HED-ID). Ectodermal dysplasias (EDs) constitute a heterogeneous group of developmental disorders affecting tissues of ectodermal origin. EDs are characterized by abnormal development of two or more ectodermal structures such as hair, teeth, nails and sweat glands, with or without any additional clinical sign. Each combination of clinical features represents a different type of ectodermal dysplasia. XL-EDA-ID is characterized by absence of sweat glands, sparse scalp hair, rare conical teeth and immunological abnormalities resulting in severe infectious diseases. & Defects in IKBKG are the cause of anhidrotic ectodermal dysplasia with immunodeficiency, osteopetrosis and lymphedema (OL- EDA-ID) [MIM:300301]. & Defects in IKBKG are a cause of immunodeficiency without anhidrotic ectodermal dysplasia [MIM:300584]; also called isolated immunodeficiency or pure immunodeficiency. & Defects in IKBKG are the cause of susceptibility to X- linked familial atypical micobacteriosis type 1 (AMCBX1) [MIM:300636]; also known as X-linked disseminated atypical mycobacterial infection type 1 or X-linked susceptibility to mycobacterial disease type 1. AMCBX1 is the X-linked recessive form of mendelian susceptibility to mycobacterial disease (MSMD). MSMD is a congenital syndrome resulting in predisposition to clinical disease caused by weakly virulent mycobacterial species, such as bacillus Calmette-Guerin vaccines and non-tuberculous, environmental mycobacteria. Patients are also susceptible to the more virulent species Mycobacterium tuberculosis. & Defects in IKBKG are the cause of recurrent isolated invasive pneumococcal disease type 2 (IPD2) [MIM:300640]. Recurrent invasive pneumococcal disease (IPD) is defined as two episodes of IPD occurring at least 1 month apart, whether caused by the same or different serotypes or strains. Recurrent IPD occurs in at least 2% of patients in most series, making IPD the most important known risk factor for subsequent IPD. & Defects in IKBKG are the cause of familial incontinentia pigmenti type II (IP2) [MIM:308300]. IP2 is a X-linked dominant disease causing death in male fetuses. In heterozygous female, it is characterized by disturbance of skin pigmentation sometimes associated with a variety of malformations of the eye, nails, teeth, skeleton, heart, and central nervous system. The prominent skin signs occur in four classic cutaneous stages: perinatal inflammatory vesicles, verrucous patches, a distinctive pattern of hyperpigmentation and dermal scarring.
Molecular Weight	48kDa

Biological Information

Immunogen

His-tagged, full-length human IKKgamma/IKK3

Host

Mouse

Specificity

IKKγ/IKK3

Isotype

IgG

Species Reactivity

Human
Mouse

Antibody Type

Monoclonal Antibody

Entrez Gene Number

NM_003639

Entrez Gene Summary

Familial incontinentia pigmenti (IP) is a genodermatosis that segregates as an X-linked dominant disorder and is usually lethal prenatally in males (The International Incontinentia Pigmenti Consortium, 2000 [PubMed 10839543]). In affected females it causes highly variable abnormalities of the skin, hair, nails, teeth, eyes, and central nervous system. The prominent skin signs occur in 4 classic cutaneous stages: perinatal inflammatory vesicles, verrucous patches, a distinctive pattern of hyperpigmentation, and dermal scarring. Cells expressing the mutated X chromosome are eliminated selectively around the time of birth, so females with IP exhibit extremely skewed X-inactivation. Familial incontinentia pigmenti is caused by mutations in the NEMO gene and is here referred to as IP2, or 'classical' incontinentia pigmenti. Sporadic incontinentia pigmenti, the so-called IP1, which maps to Xp11, is categorized as hypomelanosis of Ito (MIM 300337).[supplied by OMIM]

Gene Symbol

IKBKG
FIP3
IPD2
NEMO
IP2
Fip3p
IP1
IKKG
IKK-gamma
AMCBX1
FIP-3
IKKAP1
IP

Purification Method

Protein G Chromatography

UniProt Number

Q9Y6K9

UniProt Summary

FUNCTION: SwissProt: Q9Y6K9 # Regulatory subunit part of the IKK-signalosome complex activation. Also considered to be a mediator for TAX activation of NF-kappa-B. Could be implicated in NF-kappa-B-mediated protection from cytokine toxicity.
SIZE: 419 amino acids; 48198 Da
SUBUNIT: Interacts preferentially with IKBKB/IKK-beta but also able to interact with CHUK/IKK-alpha, IKAP, RIP and MAP3K14/NIK. Found in a complex composed of NCOA2, NCOA3, CHUK/IKKA, IKBKB/IKKB and CREBBP. Interacts with COPS3, CYLD, NALP2, TRPC4AP and LRDD. Activated through binding to HTLV-1 Tax oncoprotein.
SUBCELLULAR LOCATION: Cytoplasm. Nucleus.
TISSUE SPECIFICITY: Heart, brain, placenta, lung, liver, skeletal muscle, kidney and pancreas.
DISEASE: SwissProt: Q9Y6K9 # Defects in IKBKG are the cause of X-linked anhidrotic ectodermal dysplasia with immunodeficiency (XL-EDA-ID) [MIM:300291]; also known as hypohidrotic ectodermal dysplasia with immunodeficiency (HED-ID). Ectodermal dysplasias (EDs) constitute a heterogeneous group of developmental disorders affecting tissues of ectodermal origin. EDs are characterized by abnormal development of two or more ectodermal structures such as hair, teeth, nails and sweat glands, with or without any additional clinical sign. Each combination of clinical features represents a different type of ectodermal dysplasia. XL-EDA-ID is characterized by absence of sweat glands, sparse scalp hair, rare conical teeth and immunological abnormalities resulting in severe infectious diseases. & Defects in IKBKG are the cause of anhidrotic ectodermal dysplasia with immunodeficiency, osteopetrosis and lymphedema (OL- EDA-ID) [MIM:300301]. & Defects in IKBKG are a cause of immunodeficiency without anhidrotic ectodermal dysplasia [MIM:300584]; also called isolated immunodeficiency or pure immunodeficiency. & Defects in IKBKG are the cause of susceptibility to X- linked familial atypical micobacteriosis type 1 (AMCBX1) [MIM:300636]; also known as X-linked disseminated atypical mycobacterial infection type 1 or X-linked susceptibility to mycobacterial disease type 1. AMCBX1 is the X-linked recessive form of mendelian susceptibility to mycobacterial disease (MSMD). MSMD is a congenital syndrome resulting in predisposition to clinical disease caused by weakly virulent mycobacterial species, such as bacillus Calmette-Guerin vaccines and non-tuberculous, environmental mycobacteria. Patients are also susceptible to the more virulent species Mycobacterium tuberculosis. & Defects in IKBKG are the cause of recurrent isolated invasive pneumococcal disease type 2 (IPD2) [MIM:300640]. Recurrent invasive pneumococcal disease (IPD) is defined as two episodes of IPD occurring at least 1 month apart, whether caused by the same or different serotypes or strains. Recurrent IPD occurs in at least 2% of patients in most series, making IPD the most important known risk factor for subsequent IPD. & Defects in IKBKG are the cause of familial incontinentia pigmenti type II (IP2) [MIM:308300]. IP2 is a X-linked dominant disease causing death in male fetuses. In heterozygous female, it is characterized by disturbance of skin pigmentation sometimes associated with a variety of malformations of the eye, nails, teeth, skeleton, heart, and central nervous system. The prominent skin signs occur in four classic cutaneous stages: perinatal inflammatory vesicles, verrucous patches, a distinctive pattern of hyperpigmentation and dermal scarring.

Molecular Weight

48kDa

Product Usage Statements
Quality Assurance	routinely evaluated by immunoblot on RIPA lysates from Jurkat cells
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 on RIPA lysates from Jurkat cells

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

Storage and Shipping Information

Storage Conditions

2 years at -20°C

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-IKKg/IKK3 (mouse monoclonal IgG1)

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