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

Copper metabolism

COMMD1 is a regulator of copper homeostasis, sodium uptake, and NF-kappa-B (see MIM 164011) signaling (de Bie et al., 2005 [PubMed 16267171]).[supplied by OMIM, Sep 2009] (from NCBI)
Top mentioned proteins: ATP7B, NF-kappaB, CAN, Ubiquitin, p65
Papers on COMMD1
Copper Metabolism Domain-Containing 1 Represses the Mediators Involved in the Terminal Effector Pathways of Human Labour and Delivery.
Lappas, Melbourne, Australia. In Mol Hum Reprod, Feb 2016
STUDY HYPOTHESIS: Does Copper Metabolism MURR1 Domain 1 (COMMD1) play a role in regulating the mediators involved in the terminal processes of human labour and delivery?
COMMD7 as a novel NEMO interacting protein involved in the termination of NF-κB signaling.
Ursini et al., Napoli, Italy. In J Cell Physiol, Jan 2016
Termination of NF-κB activity on specific -κB responsive genes, which is crucial for the resolution of inflammatory responses, can be achieved by direct degradation of the chromatin-bound NF-κB subunit RelA/p65, a process mediated by a protein complex that contains Copper Metabolism Murr1 Domain 1 (COMMD1).
Downregulation of COMMD1 by miR-205 promotes a positive feedback loop for amplifying inflammatory- and stemness-associated properties of cancer cells.
Chuang et al., Taiwan. In Cell Death Differ, Dec 2015
In the present study, the analysis of microarray data revealed upregulation of NF-κB-regulated pro-inflammatory genes and downregulation of copper metabolism MURR1 domain-containing 1 (COMMD1) during the enrichment for stemness in SAS head and neck squamous-cell carcinoma (HNSCC) cells.
Disease Modeling and Gene Therapy of Copper Storage Disease in Canine Hepatic Organoids.
Schotanus et al., Utrecht, Netherlands. In Stem Cell Reports, Dec 2015
Finally, we demonstrate that successful gene supplementation in hepatic organoids of COMMD1-deficient dogs restores function and can be an effective means to cure copper storage disease.
Endosomal sorting of Notch receptors through COMMD9-dependent pathways modulates Notch signaling.
Burstein et al., Maastricht, Netherlands. In J Cell Biol, Dec 2015
Interestingly, among the 10 copper metabolism MURR1 domain containing (COMMD) family members that can associate with the CCC complex, only COMMD9 and its binding partner, COMMD5, have substantial effects on Notch.
SUMOylation-disrupting WAS mutation converts WASp from a transcriptional activator to a repressor of NF-κB response genes in T cells.
Vyas et al., Iowa City, United States. In Blood, Nov 2015
V75M, one of many disease-causing mutations occurring in SUMO*motif (72-ψψψψKDxxxxSY-83) of WASp, compromises WASp-SUMOylation, associates with COMMD1 to attenuate NF-κB signaling, and recruits histone deacetylases-6 (HDAC6) to p300-marked promoters of NF-κB response genes that pattern immunity but not inflammation.
COMMD1/Murr1 reinforces HIV-1 latent infection through IκB-α stabilization.
Okada et al., Kumamoto, Japan. In J Virol, Mar 2015
Here we show that the expression of IκB-α, an endogenous inhibitor of NF-κB, is enhanced by latent HIV-1 infection via induction of the host-derived factor COMMD1/Murr1 in myeloid cells but not in lymphoid cells by using four sets of latently HIV-1-infected cells and the respective parental cells.
Genomic Landscape of Primary Mediastinal B-Cell Lymphoma Cell Lines.
MacLeod et al., Braunschweig, Germany. In Plos One, 2014
2p15 (REL/COMMD1), 9p24 (JAK2, CD274), 16p13 (SOCS1, LITAF, CIITA); plus new or tenuously associated loci: 2p16 (MSH6), 6q23 (TNFAIP3), 9p22 (CDKN2A/B), 20p12 (PTPN1).
Functional understanding of the versatile protein copper metabolism MURR1 domain 1 (COMMD1) in copper homeostasis.
van de Sluis et al., Groningen, Netherlands. In Ann N Y Acad Sci, 2014
In dogs, a mutation in the COMMD1 gene has been found to be associated with copper toxicosis.
COMMD1 regulates inflammation and colitis-associated cancer progression.
Burstein et al., Dallas, United States. In Oncoimmunology, 2013
Copper metabolism MURR1 domain-containing 1 (COMMD1) is a negative regulator of NF-κB.
[Wilson disease - factors affecting clinical presentation].
Członkowska et al., Warsaw, Poland. In Neurol Neurochir Pol, 2013
Wilson disease (WD) is a genetic disorder with copper metabolism disturbances leading to copper accumulation in many organs with their secondary damage.
Molecular analysis of Wilson patients: direct sequencing and MLPA analysis in the ATP7B gene and Atox1 and COMMD1 gene analysis.
Wilson et al., Bron, France. In J Trace Elem Med Biol, 2012
No major role can be attributed to Atox1 and COMMD in the pathophysiology or clinical variation of Wilson disease.
Canine models of copper toxicosis for understanding mammalian copper metabolism.
Rothuizen et al., Utrecht, Netherlands. In Mamm Genome, 2012
Genetic studies in the Bedlington terrier, a dog breed affected with copper toxicosis, identified COMMD1, a gene that was previously unknown to be involved in copper metabolism.
Clusterin and COMMD1 independently regulate degradation of the mammalian copper ATPases ATP7A and ATP7B.
La Fontaine et al., Australia. In J Biol Chem, 2012
Clusterin and COMMD1 independently regulate degradation of the mammalian copper ATPases ATP7A and ATP7B.
COMMD1 (copper metabolism MURR1 domain-containing protein 1) regulates Cullin RING ligases by preventing CAND1 (Cullin-associated Nedd8-dissociated protein 1) binding.
Burstein et al., Dallas, United States. In J Biol Chem, 2011
COMMD1 (copper metabolism MURR1 domain-containing protein 1) regulates Cullin RING ligases by preventing CAND1 (Cullin-associated Nedd8-dissociated protein 1) binding.
COMMD1 regulates the delta epithelial sodium channel (δENaC) through trafficking and ubiquitination.
McDonald et al., Dunedin, New Zealand. In Biochem Biophys Res Commun, 2011
These results suggest that COMMD1 downregulates deltaENaC activity by reducing deltaENaC surface expression through promoting internalization of surface deltaENaC to an intracellular recycling pool, possibly via enhanced ubiquitination.
Copper-induced hepatitis: the COMMD1 deficient dog as a translational animal model for human chronic hepatitis.
Rothuizen et al., Utrecht, Netherlands. In Vet Q, 2011
Chronic inflammatory liver disease regardless of aetiology leads to failing regeneration and fibrosis, ending in cirrhosis.
Liver-specific Commd1 knockout mice are susceptible to hepatic copper accumulation.
van de Sluis et al., Utrecht, Netherlands. In Plos One, 2010
results provide the first genetic evidence for COMMD1 to play an essential role in hepatic copper homeostasis and present a valuable mouse model for further understanding of the molecular mechanisms underlying hepatic copper homeostasis
COMMD proteins: COMMing to the scene.
Burstein et al., Ann Arbor, United States. In Cell Mol Life Sci, 2007
COMM Domain-containing or COMMD proteins are a recently discovered group of factors defined by the presence of a unique motif in their extreme carboxy termini (Copper metabolism MURR1, or COMM domain).
The gene product Murr1 restricts HIV-1 replication in resting CD4+ lymphocytes.
Nabel et al., Bethesda, United States. In Nature, 2004
Murr1, a gene product known previously for its involvement in copper regulation, inhibits HIV-1 growth in unstimulated CD4+ T cells
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