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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase complex-associated protein

The protein encoded by this gene is a scaffold protein and a regulator for 3 different kinases involved in proinflammatory signaling. This encoded protein can bind NF-kappa-B-inducing kinase (NIK) and IKKs through separate domains and assemble them into an active kinase complex. Mutations in this gene have been associated with familial dysautonomia. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, POLYMERASE, HAD, AGE, elastin
Papers using Dys antibodies
Tubulin modifications and their cellular functions.
Baccei Mark L., In PLoS ONE, 2007
... siRNA candidates for IKBKAP were identified using the Whitehead Institute for Biomedical Reseach's website ( ...
The synaptic vesicle protein SV2 is complexed with an alpha5-containing laminin on the nerve terminal surface.
Andreu Antoni L., In PLoS ONE, 1999
... The Dys-COOH RNAi transgenic flies were described in ...
Papers on Dys
Phosphatidylserine enhances IKBKAP transcription by activating the MAPK/ERK signaling pathway.
Ast et al., Tel Aviv-Yafo, Israel. In Hum Mol Genet, Feb 2016
FD is caused by a point mutation in the IKBKAP gene encoding the IKAP protein, resulting in decreased protein levels.
Sensory and Autonomic Deficits in a New Humanized Mouse Model of Familial Dysautonomia.
Dragatsis et al., Boston, United States. In Hum Mol Genet, Feb 2016
FD is caused by an mRNA splicing mutation in intron 20 of the IKBKAP gene that results in a tissue-specific skipping of exon 20 and a corresponding reduction of the inhibitor of kappaB kinase complex-associated protein (IKAP), also known as Elongator complex protein 1 (ELP1).
Diagnosis of Muscular Dystrophy Using Western Blot with Micro-sample of Muscle.
Jiao et al., Beijing, China. In Zhongguo Yi Xue Ke Xue Yuan Xue Bao, Jan 2016
Compared with the Results of immunohistochemical staining detected the severe abnormal expressions of Dys-R,Dys-C,and Dys-N in the specimens,we did not detect the corresponding target band in WB.
Up-regulation of SRPK1 in non-small cell lung cancer promotes the growth and migration of cancer cells.
Chen et al., Shanghai, China. In Tumour Biol, Jan 2016
UNASSIGNED: Dys-regulation of serine-arginine protein kinase 1 (SRPK1) has been reported in non-small cell lung cancer (NSCLC).
microRNAs and Endothelial (Dys) Function.
Santulli, New York City, United States. In J Cell Physiol, Jan 2016
UNASSIGNED: Accumulating evidence indicates that microRNAs (miRs) - non-coding RNAs that can regulate gene expression via translational repression and/or post-transcriptional degradation - are becoming one of the most fascinating areas of physiology, given their fundamental roles in countless pathophysiological processes.
IKAP: A heuristic framework for inference of kinase activities from Phosphoproteomics data.
Klabunde et al., Martinsried, Germany. In Bioinformatics, Jan 2016
Dimerization of elongator protein 1 is essential for Elongator complex assembly.
Long et al., Tianjin, China. In Proc Natl Acad Sci U S A, Sep 2015
The molecular hallmark of familial dysautonomia (FD) is the splicing mutation of Elp1 [also known as IκB kinase complex-associated protein (IKAP)] in the nervous system that is believed to be the primary cause of the devastating symptoms of this disease.
Liver Disease and Hemostatic (Dys)function.
Tripodi, Milano, Italy. In Semin Thromb Hemost, Jul 2015
Cirrhosis presents with decreased procoagulant factors as a consequence of the impaired synthetic capacity of the liver.
The facts about sexual (Dys)function in schizophrenia: an overview of clinically relevant findings.
Knegtering et al., Groningen, Netherlands. In Schizophr Bull, May 2015
A limited number of studies have evaluated sexual functioning in patients with schizophrenia.
Familial Dysautonomia (FD) Human Embryonic Stem Cell Derived PNS Neurons Reveal that Synaptic Vesicular and Neuronal Transport Genes Are Directly or Indirectly Affected by IKBKAP Downregulation.
Weil et al., Tel Aviv-Yafo, Israel. In Plos One, 2014
A splicing mutation in the IKBKAP gene causes Familial Dysautonomia (FD), affecting the IKAP protein expression levels and proper development and function of the peripheral nervous system (PNS).
Current treatments in familial dysautonomia.
Kaufmann et al., New York City, United States. In Expert Opin Pharmacother, 2014
The disease is caused by a point mutation in the IKBKAP gene that affects the splicing of the elongator-1 protein (ELP-1) (also known as IKAP).
Various methods available for detection of apoptotic cells--a review.
Kumaraswamy et al., Bengaluru, India. In Indian J Cancer, 2013
Dys regulation of apoptosis can play a primary or secondary role leading to cancer whereas excessive apoptosis contributes to neuro degeneration, autoimmunity, AIDS, and ischemia.
Large-scale screening using familial dysautonomia induced pluripotent stem cells identifies compounds that rescue IKBKAP expression.
Studer et al., New York City, United States. In Nat Biotechnol, 2012
We tested 6,912 small-molecule compounds and characterized eight that rescued expression of IKBKAP, the gene responsible for FD.
Nutraceutical-mediated restoration of wild-type levels of IKBKAP-encoded IKAP protein in familial dysautonomia-derived cells.
Rubin et al., United States. In Mol Nutr Food Res, 2012
Combined treatment with epigallocatechin gallate and genistein synergistically upregulates wild-type IKBKAP-encoded RNA and protein levels in familial dysautonomia-derived cells.
IKAP/Elp1 is required in vivo for neurogenesis and neuronal survival, but not for neural crest migration.
Lefcort et al., Bozeman, United States. In Plos One, 2011
IKAP plays pleiotropic roles in both the peripheral and central nervous systems
Effects of IKAP/hELP1 deficiency on gene expression in differentiating neuroblastoma cells: implications for familial dysautonomia.
Weil et al., Tel Aviv-Yafo, Israel. In Plos One, 2010
IKAP/hELP1 deficiency has an effect on gene expression in differentiating neuroblastoma cells, and possibly on familial dysautonomia
New dystrophin/dystroglycan interactors control neuron behavior in Drosophila eye.
Shcherbata et al., Göttingen, Germany. In Bmc Neurosci, 2010
Nrk, mbl, capt and Cam genetically interact with dystrophin and/or dystroglycan in the process of axon path-finding in the eye.
Deletion of exon 20 of the Familial Dysautonomia gene Ikbkap in mice causes developmental delay, cardiovascular defects, and early embryonic lethality.
Dragatsis et al., Memphis, United States. In Plos One, 2010
IKAP is essential for expression of specific genes involved in cardiac morphogenesis, and cardiac failure is the likely cause of abnormal vascular development and embryonic lethality; deletion of exon 20 abolishes gene function
Modelling pathogenesis and treatment of familial dysautonomia using patient-specific iPSCs.
Studer et al., York, United States. In Nature, 2009
Familial dysautonomia (FD) is a rare but fatal peripheral neuropathy, caused by a point mutation in the IKBKAP gene involved in transcriptional elongation.
IKAP is a scaffold protein of the IkappaB kinase complex.
Baeuerle et al., San Francisco, United States. In Nature, 1998
This latter component is a new protein, termed IKK-complex-associated protein (IKAP), which can bind NIK and IKKs and assemble them into an active kinase complex.
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