Familial incontinentia pigmenti (IP) is a genodermatosis that segregates as an X-linked dominant disorder and is usually lethal prenatally in males . 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
Liquid. Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
WB Suggested Anti-IKBKG Antibody Titration: 1.25ug/ml ELISA Titer: 1:312500 Positive Control: HepG2 cell lysateIKBKG is strongly supported by BioGPS gene expression data to be expressed in Human HepG2 cells
Lanes: 1. 100 ug mouse testis lysate 2. 100 ug HeLa cell lysate Primary Antibody Dilution: 1:800 Secondary Antibody: Anti-rabbit-AP Secondary Antibody Dilution: 1:10000 Gene Name: IKBKG Submitted by: Andreia Carvalho, Instituto de Biologia Molecular e Celular, Universidade do Porto (IBMC-UP)/Organelle Biogenesis and Function (OBF) Group
IKBKG antibody - middle region (ARP30005_T100) in Human HepG2 using Western Blot
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