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

CDGSH iron sulfur domain 2

Eris, WFS2
The protein encoded by this gene is a zinc finger protein that localizes to the endoplasmic reticulum. The encoded protein binds an iron/sulfur cluster and may be involved in calcium homeostasis. Defects in this gene are a cause of Wolfram syndrome 2. [provided by RefSeq, Mar 2011] (from NCBI)
Top mentioned proteins: TBK1, WFS1, Interferon Regulatory Factor-3, ACID, CAN
Papers on Eris
The emerging roles of the STING adaptor protein in immunity and diseases.
Review
New
Wang et al., Shanghai, China. In Immunology, Jan 2016
An emerging paradigm for responding to cytosolic DNAs centers on the ER-resident protein stimulator of interferon genes (STING, also known as MITA, ERIS or MPYS), the hub adaptor of the recently identified DNA sensors.
Dysregulation of Mitochondrial Functions and Osteogenic Differentiation in Cisd2-Deficient Murine Induced Pluripotent Stem Cells.
New
Chiou et al., Taipei, Taiwan. In Stem Cells Dev, Dec 2015
Cisd2, which regulates mitochondrial electron transport, has been recently identified as the causative gene of WFS2.
Antiviral role of grouper STING against iridovirus infection.
New
Qin et al., Guangzhou, China. In Fish Shellfish Immunol, Nov 2015
Stimulator of interferon genes (STING, also known as MITA, ERIS, MPYS or TMEM173) has been identified as a central component in the innate immune response to cytosolic DNA and RNA derived from different pathogens.
PPM1A regulates antiviral signaling by antagonizing TBK1-mediated STING phosphorylation and aggregation.
New
Sun et al., Beijing, China. In Plos Pathog, Mar 2015
Stimulator of interferon genes (STING, also known as MITA and ERIS) is critical in protecting the host against DNA pathogen invasion.
The E3 ubiquitin ligase AMFR and INSIG1 bridge the activation of TBK1 kinase by modifying the adaptor STING.
Impact
Wang et al., Shanghai, China. In Immunity, 2015
Stimulator of interferon genes (STING, also known as MITA, ERIS, or MPYS) is essential for host immune responses triggered by microbial DNAs.
A calcium-dependent protease as a potential therapeutic target for Wolfram syndrome.
Urano et al., Tokyo, Japan. In Proc Natl Acad Sci U S A, 2015
Despite the underlying importance of ER dysfunction in Wolfram syndrome and the identification of two causative genes, Wolfram syndrome 1 (WFS1) and Wolfram syndrome 2 (WFS2), a molecular mechanism linking the ER to death of neurons and β cells has not been elucidated.
NLRC3, a member of the NLR family of proteins, is a negative regulator of innate immune signaling induced by the DNA sensor STING.
Review
Impact
Ting et al., Chapel Hill, United States. In Immunity, 2014
Stimulator of interferon genes (STING, also named MITA, MYPS, or ERIS) is an intracellular DNA sensor that induces type I interferon through its interaction with TANK-binding kinase 1 (TBK1).
Genetic studies in Drosophila and humans support a model for the concerted function of CISD2, PPT1 and CLN3 in disease.
Grotewiel et al., Richmond, United States. In Biol Open, 2013
WFS1 and WFS2 are caused by recessive mutations in the genes Wolfram Syndrome 1 (WFS1) and CDGSH iron sulfur domain 2 (CISD2), respectively.
NET23/STING promotes chromatin compaction from the nuclear envelope.
Schirmer et al., Edinburgh, United Kingdom. In Plos One, 2013
One of these, NET23 (also called STING, MITA, MPYS, ERIS, Tmem173), strongly promoted chromatin compaction.
A novel CISD2 intragenic deletion, optic neuropathy and platelet aggregation defect in Wolfram syndrome type 2.
Franzese et al., Napoli, Italy. In Bmc Med Genet, 2013
The disease gene for WFS2 is CISD2.
Predicting the impact of deleterious mutations in the protein kinase domain of FGFR2 in the context of function, structure, and pathogenesis--a bioinformatics approach.
Chakraborty et al., Vellore, India. In Appl Biochem Biotechnol, 2013
Tolerance index, position-specific independent count score, change in free energy score (ΔΔG), Eris and FoldX indicated that seven mutations were found to be deleterious and may alter the protein function and structure.
Wolfram syndrome 1 and Wolfram syndrome 2.
Review
Di Bella et al., Messina, Italy. In Curr Opin Pediatr, 2012
The CISD2-encoded protein ERIS (endoplasmic reticulum intermembrane small protein) also localizes to ER, but does not interact directly with wolframin.
STING is a direct innate immune sensor of cyclic di-GMP.
Impact
Vance et al., Berkeley, United States. In Nature, 2011
In addition, a transmembrane protein called STING (stimulator of IFN genes; also known as MITA, ERIS, MPYS and TMEM173) functions as an essential signalling adaptor, linking the cytosolic detection of DNA to the TBK1-IRF3 signalling axis.
Activation of STAT6 by STING is critical for antiviral innate immunity.
Impact
Jiang et al., Beijing, China. In Cell, 2011
Viruses or cytoplasmic nucleic acids trigger STING (also named MITA/ERIS) to recruit STAT6 to the endoplasmic reticulum, leading to STAT6 phosphorylation on Ser(407) by TBK1 and Tyr(641), independent of JAKs.
A role for the CISD2 gene in lifespan control and human disease.
Review
GeneRIF
Tsai et al., Taipei, Taiwan. In Ann N Y Acad Sci, 2010
CISD2 has a role in lifespan control and disease [review]
Crystal structure of Miner1: The redox-active 2Fe-2S protein causative in Wolfram Syndrome 2.
GeneRIF
Paddock et al., San Diego, United States. In J Mol Biol, 2009
The authors show that Miner1 is a homodimer harboring two redox-active 2Fe-2S clusters, indicating for the first time an association of a redox-active FeS protein with Wolfram Syndrome 2.
A homozygous mutation in a novel zinc-finger protein, ERIS, is responsible for Wolfram syndrome 2.
GeneRIF
Shiang et al., Richmond, United States. In Am J Hum Genet, 2007
A single missense mutation was identified in a novel, highly conserved zinc-finger gene, ZCD2, in three consanguineous families of Jordanian descent with Wolfram syndrome (WFS).
Wolfram syndrome: phenotype and novel mutation in two Taiwanese siblings.
GeneRIF
Chi et al., Taiwan. In J Formos Med Assoc, 2003
Novel mutation, new phenotypic variant with no diabetes insipidus, presence of peptic ulcer disease, platelet aggregation defect
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