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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 27 Nov 2014.

Inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase gamma

Incontinentia Pigmenti, NEMO, IPI, IKKgamma, IP2
This gene encodes the regulatory subunit of the inhibitor of kappaB kinase (IKK) complex, which activates NF-kappaB resulting in activation of genes involved in inflammation, immunity, cell survival, and other pathways. Mutations in this gene result in incontinentia pigmenti, hypohidrotic ectodermal dysplasia, and several other types of immunodeficiencies. Multiple transcript variants encoding different isoforms have been found for this gene. A pseudogene highly similar to this locus is located in an adjacent region of the X chromosome. [provided by RefSeq, Aug 2011] (from NCBI)
Top mentioned proteins: NF-kappaB, CAN, HAD, Ubiquitin, V1a
Papers using Incontinentia Pigmenti antibodies
Bioinformatics enrichment tools: paths toward the comprehensive functional analysis of large gene lists
Martelli Fabio, In PLoS ONE, 2008
... The Refseq ids were converted to IPI ids using an online server ...
Control of canonical NF-κB activation through the NIK-IKK complex pathway
May Michael J. et al., In Oncogene, 2007
... Anti-RET, IKKα, p50, NIK, TRAF3, TRAF2, RelB, and NEMO were from Santa Cruz Biotechnology (Santa Cruz, CA) ...
Papers on Incontinentia Pigmenti
Relationship between irradiation-induced neuro-inflammatory environments and impaired cognitive function in the developing brain of mice.
Cheng et al., In Int J Radiat Biol, 26 Dec 2014
The cytoplasm to nuclei translocation of Nuclear factor kappa B (NF-κB), and the protein expressions of IkappaB-alpha (IκB-α), NF-κB essential modulator (NEMO), p53-induced protein with a death domain (PIDD), TNF-α and IL-1β were examined by Western blotting.
Ubiquitination profiling identifies sensitivity factors for IAP antagonist treatment.
Vucic et al., In Biochem J, 21 Dec 2014
Analysis of early timepoints revealed that IAP antagonist treatment stimulated rapid ubiquitination of NF-kB signaling proteins including TRAF2, HOIL1, NEMO as well as c-IAP1 autoubiquitination.
Disulfide-Mediated Stabilization of the IκB Kinase Binding Domain of NF-κB Essential Modulator (NEMO).
Whitty et al., In Biochemistry, 15 Dec 2014
UNLABELLED: Human NEMO (NF-κB essential modulator) is a 419 residue scaffolding protein that, together with catalytic subunits IKKα and IKKβ, forms the IκB kinase (IKK) complex, a key regulator of NF-κB pathway signaling.
An RCOR1 loss-associated gene expression signature identifies a prognostically significant DLBCL subgroup.
Steidl et al., Vancouver, Canada. In Blood, 13 Dec 2014
Additionally, we discovered that within the IPI low risk group, the gene signature provides additional prognostic value that was independent of the cell-of-origin phenotype.
Rhbdd3 controls autoimmunity by suppressing the production of IL-6 by dendritic cells via K27-linked ubiquitination of the regulator NEMO.
Cao et al., Shanghai, China. In Nat Immunol, Jul 2014
Rhbdd3-deficient mice spontaneously developed autoimmune diseases characterized by an increased abundance of the TH17 subset of helper T cells and decreased number of regulatory T cells due to the increase in IL-6 from DCs. Rhbdd3 directly bound to Lys27 (K27)-linked polyubiquitin chains on Lys302 of the modulator NEMO (IKKγ) via the ubiquitin-binding-association (UBA) domain in endosomes.
Hematopoietic Cell Transplantation for Plasmablastic Lymphoma: a review.
Re et al., Providence, United States. In Biol Blood Marrow Transplant, Jul 2014
Multiple adverse prognostic factors have been identified including HIV-negativity, MYC gene rearrangement, high-risk international prognostic index (IPI), and not achieving complete remission (CR) post-induction therapy.
Prognostic Factors For Diffuse Large B Cell Lymphoma In the R(X)CHOP Era.
Witzig et al., Rochester, United States. In Ann Oncol, Apr 2014
RESULTS: The IPI retains its validity in the era of RCHOP, although with limited ability to predict those with <50% chance of long-term survival.
Incontinentia pigmenti in an XY boy: case report and review of the literature.
Moroz et al., In J Cutan Med Surg, Mar 2014
OBJECTIVE: To report a case of a surviving XY male with the common IKBKG (NEMO) gene deletion confirming IP.
Incontinentia pigmenti.
Bau et al., Porto Alegre, Brazil. In An Bras Dermatol, Jan 2014
Incontinentia pigmenti is a rare genodermatosis in which the skin involvement occurs in all patients.
Chronic Inflammation and Angiogenic Signaling Axis Impairs Differentiation of Dental-Pulp Stem Cells.
Alapati et al., Chicago, United States. In Plos One, Dec 2013
Interestingly, DPSC pretreated with Nemo binding domain (NBD) peptide (a cell permeable NF-κB inhibitor) significantly ameliorated TNF-α- and/or VEGF-induced proliferation and the shortening of telomere length.
Molecular control of the NEMO family of ubiquitin-binding proteins.
Cohen et al., Dundee, United Kingdom. In Nat Rev Mol Cell Biol, Oct 2013
Research over the past decade has revealed how NF-κB essential modulator (NEMO; also known as IKKγ) regulates the IKKα-IKKβ signalling axis in the innate immune system.
Histone methyltransferase Ash1l suppresses interleukin-6 production and inflammatory autoimmune diseases by inducing the ubiquitin-editing enzyme A20.
Cao et al., Hangzhou, China. In Immunity, Oct 2013
Ash1l suppressed NF-κB, mitogen-activated protein kinase (MAPK) pathways, and subsequent IL-6 production via facilitating A20-mediated NF-κB signal modulator NEMO and transducer TRAF6 deubiquitination.
OTULIN antagonizes LUBAC signaling by specifically hydrolyzing Met1-linked polyubiquitin.
Komander et al., Cambridge, United Kingdom. In Cell, Jul 2013
We show that OTULIN binds LUBAC and that overexpression of OTULIN prevents TNFα-induced NEMO association with ubiquitinated RIPK1.
Ectodermal dysplasia: a genetic review.
Prashanth et al., Mysore, India. In Int J Clin Pediatr Dent, 2012
The history and lessons learned from hypohidrotic ectodermal dysplasia (HED) may serve as an example for unraveling of the cause and pathogenesis of other ectodermal dysplasia syndromes by demonstrating that phenotypically identical syndromes can be caused by mutations in different genes (EDA, EDAR, EDARADD), that mutations in the same gene can lead to different phenotypes and that mutations in the genes further downstream in the same signaling pathway (NEMO) may modify the phenotype quite profoundly.
NEMO ensures signaling specificity of the pleiotropic IKKβ by directing its kinase activity toward IκBα.
Hoffmann et al., San Diego, United States. In Mol Cell, 2012
Data show that NEMO forms a complex with IKKbeta and IkappaBalpha.
Analysis of nuclear factor-κB (NF-κB) essential modulator (NEMO) binding to linear and lysine-linked ubiquitin chains and its role in the activation of NF-κB.
Dikic et al., Frankfurt am Main, Germany. In J Biol Chem, 2012
Data indicate that modification of NEMO with linear di-ubiquitin is sufficient for full NF-kappaB activation.
NEMO expression in human hepatocellular carcinoma and its association with clinical outcome.
Pichler et al., Graz, Austria. In Hum Pathol, 2012
Although low NEMO expression is correlated with a poor 5-year overall survival in patients with hepatocellular carcinoma, NEMO cannot be regarded as an independent prognostic marker for predicting the clinical outcome of patients suffering from HCC.
Frequent somatic mosaicism of NEMO in T cells of patients with X-linked anhidrotic ectodermal dysplasia with immunodeficiency.
Heike et al., Kyoto, Japan. In Blood, 2012
These data indicate that the frequency of somatic mosaicism of NEMO is high in X-linked anhidrotic ectodermal dysplasia with immunodeficiency patients.
Viral mediated redirection of NEMO/IKKγ to autophagosomes curtails the inflammatory cascade.
Brune et al., Hamburg, Germany. In Plos Pathog, 2012
Murine cytomegalovirus inhibits the inflammatory cascade by blocking Toll-like receptor and IL-1 receptor-dependent NF-kappaB activation through an interaction of the viral M45 protein with the NF-kappaB essential modulator.
Exploiting cancer cell vulnerabilities to develop a combination therapy for ras-driven tumors.
Cichowski et al., Boston, United States. In Cancer Cell, 2011
We show that agents that enhance proteotoxic stress, including the HSP90 inhibitor IPI-504, induce tumor regression in aggressive mouse models, but only when combined with rapamycin.
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