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Wählen Sie konfigurierbare Panels & Premixed-Kits - ODER - Kits für die zelluläre Signaltransduktion & MAPmates™
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Kits für die zelluläre Signaltransduktion & MAPmates™
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Die folgenden MAPmates™ sollten nicht zusammen analysiert werden: -MAPmates™, die einen unterschiedlichen Assaypuffer erfordern. -Phosphospezifische und MAPmate™ Gesamtkombinationen wie Gesamt-GSK3β und Gesamt-GSK3β (Ser 9). -PanTyr und locusspezifische MAPmates™, z.B. Phospho-EGF-Rezeptor und Phospho-STAT1 (Tyr701). -Mehr als 1 Phospho-MAPmate™ für ein einziges Target (Akt, STAT3). -GAPDH und β-Tubulin können nicht mit Kits oder MAPmates™, die panTyr enthalten, analysiert werden.
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Gewähltes Kit
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96-Well Plate
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48-602MAG
Buffer Detection Kit for Magnetic Beads
1 Kit
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05-631
Sigma-AldrichAnti-IKKγ Antibody
Anti-IKKγ Antibody is an antibody against IKKγ for use in WB.
More>>Anti-IKKγ Antibody is an antibody against IKKγ for use in WB. Less<<
Anti-IKKγ Antibody: SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
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]
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
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
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.
Oncoprotein Suppression of Tumor Necrosis Factor-induced NF{kappa}B Activation Is Independent of Raf-controlled Pathways Hanson, J. L., et al J Biol Chem, 278:34910-34917 (2003)
2003
