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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
Nemo-like kinase regulates postnatal skeletal homeostasis.
Zanotti et al., Farmington, United States. In J Cell Physiol, 30 Nov 2014
Nemo-like kinase (Nlk) is related to the mitogen-activated protein (MAP) kinases and known to regulate signaling pathways involved in osteoblastogenesis.
NEMO is essential for Kaposi's sarcoma-associated herpesvirus-encoded vFLIP K13-induced gene expression and protection against death receptor-induced cell death, and its N-terminal 251 residues are sufficient for this process.
Chaudhary et al., Los Angeles, United States. In J Virol, Jun 2014
Subsequent studies revealed that K13 also activates the NF-κB pathway by binding to the NEMO/inhibitor of NF-κB (IκB) kinase gamma (IKKγ) subunit of an IKK complex and uses this pathway to modulate the expression of genes involved in cellular survival, proliferation, and the inflammatory response.
MicroRNA-23a expression in paraffin-embedded specimen correlates with overall survival of diffuse large B-cell lymphoma.
Li et al., Xinxiang, China. In Med Oncol, Apr 2014
No significant association was observed between the miR-23a expression level and clinical features such as age, gender, Ann Arbor stage, performance status, lactate dehydrogenase, extranodal sites and International Prognostic Index score (IPI).
A172: Metaphyseal Chondrodysplasia, Ectodermal Dysplasia, Short Stature, Hypergammaglobulinemia, and Spontaneous Inflammation Without Infections in an Extended Family Due to Mutation in NFKB1A.
Buzzell et al., Milwaukee, United States. In Arthritis Rheumatol, Mar 2014
Defects in the NF-kB essential modifier pathway, or NEMO, are associated with an immune deficiency characterized by ectodermal dysplasia.
A128: hierarchical clustering methodology for exploration of proteomic profile in tears: seeking for markers of uveitis associated with juvenile idiopathic arthritis.
Chasnyk et al., Washington, D.C., United States. In Arthritis Rheumatol, Mar 2014
Proteins were identified from the mass spectra results with Proteome Discoverer software for protein database search using the International Protein Index (IPI) Human Protein Database (version 1.79).
Is interpregnancy interval associated with cardiovascular risk factors in later life? A cohort study.
Howe et al., Bristol, United Kingdom. In Bmj Open, Dec 2013
Conversely, it is also possible that a long interpregnancy interval (IPI) may reflect subfertility, which has been found to be associated with cardiovascular disease (CVD).
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.
Discovery and development of heat shock protein 90 inhibitors as anticancer agents: a review of patented potent geldanamycin derivatives.
Pae et al., Seoul, South Korea. In Expert Opin Ther Pat, Aug 2013
Currently, several GM derivatives such as 17-AAG, 17-(2-dimethylaminoethyl)amino-17-demethoxygeldanamycin, IPI-493, and IPI-504 are being progressively developed toward clinical application.
Genetic background of nonsyndromic oligodontia: a systematic review and meta-analysis.
Jabir et al., Gießen, Germany. In J Orofac Orthop, Jul 2013
All these genes vary both in terms of number of identified mutations and in terms of number of documented patients: 33 mutations and 93 patients are on record for PAX9, 10 mutations and 51 patients for EDA, 12 mutations and 33 patients for MSX1, 6 mutations and 17 patients for AXIN2, and 1 mutation in 1 patient for EDARADD, NEMO, and KRT17 each.
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.
Mendelian predisposition to herpes simplex encephalitis.
Casanova et al., New York City, United States. In Handb Clin Neurol, 2012
Autosomal recessive STAT-1 deficiency and X-linked NEMO deficiency were found in children with both mycobacterial disease and HSE.
Systematic review of central nervous system anomalies in incontinentia pigmenti.
Obradović et al., Belgrade, Serbia. In Orphanet J Rare Dis, 2012
The objective of this study was to present a systematic review of the central nervous system (CNS) types of anomalies and to consider the possibility to include CNS anomalies in Incontinentia pigmenti (IP) criteria.
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.
FADD prevents RIP3-mediated epithelial cell necrosis and chronic intestinal inflammation.
Pasparakis et al., Köln, Germany. In Nature, 2011
Epithelial-specific inhibition of CYLD, a deubiquitinase that regulates cellular necrosis, prevented colitis development in FADD(IEC-KO) but not in NEMO(IEC-KO) mice, showing that different mechanisms mediated death of colonic epithelial cells in these two models.
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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