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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 11 Dec 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
Supplier
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
Supplier
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
Gliotoxin suppresses NF-ĸB activation by selectively inhibiting linear ubiquitin chain assembly complex (LUBAC).
New
Nagano et al., In Acs Chem Biol, 10 Jan 2015
UNLABELLED: Linear ubiquitin chain, which consists of ubiquiitin molecules linked via their N- and C- termini, is formed by linear ubiquitin chain assembly complex (LUBAC) composed of HOIP, HOIL-1L and SHARPIN, and conjugation of linear ubiquitin chain on NF-ĸB essential modulator (NEMO) is deeply involved in NF-ĸB activation induced by various signals.
Novel Lys63-Linked Ubiquitination of IKKβ Induces STAT3 Signaling.
New
Donoghue et al., San Diego, United States. In Cell Cycle, 08 Jan 2015
NFκB activation requires Lys63-linked (K63-linked) ubiquitination of upstream proteins such as NEMO or TAK1, forming molecular complexes with membrane-bound receptors.
Resolving clinical diagnoses for syndromic cleft lip and/or palate phenotypes using whole-exome sequencing.
New
Briceno et al., Southampton, United Kingdom. In Clin Genet, 01 Jan 2015
These include the molecular diagnosis of an individual with Nager syndrome and a family exhibiting an atypical Incontinentia Pigmenti phenotype with a missense mutation in IKBKG.
Switching to BCL-6 Negativity in Relapsed Diffuse Large B Cell Lymphoma Correlated with More Aggressive Disease Course.
New
Mihaljevic et al., Belgrade, Serbia. In Indian J Hematol Blood Transfus, 31 Dec 2014
Bone marrow infiltration and high IPI risk were more often present in BCL-6(-) patients.
Mendelian susceptibility to mycobacterial disease: Genetic, immunological, and clinical features of inborn errors of IFN-γ immunity.
Review
New
Casanova et al., New York City, United States. In Semin Immunol, 26 Nov 2014
Since 1996, nine MSMD-causing genes, including seven autosomal (IFNGR1, IFNGR2, STAT1, IL12B, IL12RB1, ISG15, and IRF8) and two X-linked (NEMO, and CYBB) genes have been discovered.
Novel Agents in the Treatment of Chronic Lymphocytic Leukemia: A Review About the Future.
Review
New
Abdul-Hay et al., New York City, United States. In Clin Lymphoma Myeloma Leuk, Oct 2014
In this review article we discuss in detail several of the novel agents that are being studied or approved for the treatment of CLL including: phosphatidylinositol 3-kinase inhibitors (idelalisib and IPI-145), Bruton tyrosine kinase inhibitors (ibrutinib), B cell lymphoma 2 inhibitors (ABT-263 and ABT-199), new anti-CD20 monoclonal antibodies (obinutuzumab), cyclin-dependent kinase inhibitors (flavopiridol and dinaciclib), immunomodulators (lenalidomide) and chimeric antigen receptor T-cell therapy.
Rhbdd3 controls autoimmunity by suppressing the production of IL-6 by dendritic cells via K27-linked ubiquitination of the regulator NEMO.
New
Impact
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.
Review
New
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.
Incontinentia pigmenti in an XY boy: case report and review of the literature.
Review
New
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.
Molecular control of the NEMO family of ubiquitin-binding proteins.
Review
New
Impact
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.
New
Impact
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.
New
Impact
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.
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
Impact
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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