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

HECT, UBA and WWE domain containing 1

Mule, ARF-BP1, HUWE1, HectH9, ARF-binding protein, UREB1
This gene encodes a member of the HECT E3 ubiquitin ligase family. The HECT domain lies in the C-terminus and contains the active-site cysteine which forms an intermediate ubiquitin-thioester bond. E3 family members are divided into three subfamilies based on their protein-protein interaction domains; this gene encodes a member of the SI(ngle)-HECT E3 subfamily. In lung, breast, and colorectal carcinomas, this gene is highly expressed. Mutations in this gene has been found in 3 unrelated families with X-linked syndromic mental retardation, Turner type. [provided by RefSeq, Nov 2009] (from NCBI)
Top mentioned proteins: Ubiquitin, p16, CAN, 4E-BP1, p53
Papers using Mule antibodies
Bcl2 inhibits abasic site repair by down-regulating APE1 endonuclease activity
Deng Xingming et al., In Molecular Cancer, 2007
... Anti-Mule antibody was purchased from Bethyl Laboratories, INC ...
Emerging roles for ubiquitin and protein degradation in neuronal function
Schuman Erin M. et al., In Frontiers in Molecular Neuroscience, 2006
... (Billerica, MA, USA); PSMD9 (sc-10670), 14-3-3γ (sc-731) from Santa Cruz Biotechnology (Santa Cruz, CA, USA); HUWE1 (A300-486A) from Bethyl (Montgomery, TX, USA); tubulin ...
Papers on Mule
Mcl-1 dynamics influence mitotic slippage and death in mitosis.
Taylor et al., Manchester, United Kingdom. In Oncotarget, Feb 2016
However, this degradation does not require the activity of either APC/C-Cdc20, FBW7 or MULE, three separate E3 ubiquitin ligases implicated in targeting Mcl-1 for degradation.
ATM and SIRT6/SNF2H Mediate Transient H2AX Stabilization When DSBs Form by Blocking HUWE1 to Allow Efficient γH2AX Foci Formation.
Yoshioka et al., Tokyo, Japan. In Cell Rep, Jan 2016
Synthesized H2AX ordinarily underwent degradation through poly-ubiquitination mediated by the E3 ligase HUWE1; however, H2AX ubiquitination was transiently halted upon DSB formation.
Genotype-phenotype characterization in 13 individuals with chromosome Xp11.22 duplications.
Chen et al., Canada. In Am J Med Genet A, Jan 2016
In total, we have collected data on nine individuals with duplications overlapping the distal duplication region containing SHROOM4 and DGKK and eight individuals overlapping the proximal region including HUWE1.
Spatial control of Shoc2-scaffold-mediated ERK1/2 signaling requires remodeling activity of the ATPase PSMC5.
Galperin et al., Lexington, United States. In J Cell Sci, Jan 2016
The amplitude of the ERK1/2 signals transduced through the complex is fine-tuned by the HUWE1-mediated ubiquitylation of Shoc2 and its signaling partner RAF-1.
Xp11.22 Microduplications including HUWE1: Case Report and Literature Review.
Piccolo et al., Parma, Italy. In Neuropediatrics, Dec 2015
Within this region, only one gene, the HUWE1 gene, coding the E3 ubiquitin protein ligase, turned out to be duplicated in all previously described patients.
Regulation of mitochondrial morphology and function by stearoylation of TFR1.
Teleman et al., Heidelberg, Germany. In Nature, Oct 2015
This leads to reduced ubiquitination of mitofusin via HUWE1, thereby promoting mitochondrial fusion and function.
Mutator and MULE Transposons.
Lisch, In Microbiol Spectr, Apr 2015
The Mutator system of transposable elements (TEs) is a highly mutagenic family of transposons in maize.
The role of the ubiquitin proteasome system in cerebellar development and medulloblastoma.
Marzban et al., Winnipeg, Canada. In Mol Brain, 2014
We propose the hypothesis that proteasomal activity is essential to regulate the critical transition between proliferating granule cells and differentiated granule cells and that proteasome dysfunction may lead to MB. Proteasome dysfunction could also account for various mutations in MBs resulting from deficiencies in DNA checkpoint and repair mechanisms prior to development of MBs.Data showing a role for the ubiquitin ligases β-TrCP, FBW7, Huwe1, and SKP2 in MBs suggest the possibility of a classification of MBs based on the expression (over expression or under expression) of specific ubiquitin ligases which function as oncogenes, tumor suppressors or cell cycle regulators.
Huwe1 interacts with Gadd45b under oxygen-glucose deprivation and reperfusion injury in primary Rat cortical neuronal cells.
Li et al., Chongqing, China. In Mol Brain, 2014
Here, using an oxygen-glucose deprivation and reperfusion (OGD/R) model, we identified Huwe1/Mule/ARF-BP1, a HECT domain containing ubiquitin ligase, involved in the control of Gadd45b protein level.
Monitoring regulation of DNA repair activities of cultured cells in-gel using the comet assay.
Parsons et al., Liverpool, United Kingdom. In Front Genet, 2013
For example, we have shown that the E3 ubiquitin ligase Mule, the tumor suppressor protein ARF, and the deubiquitylation enzyme USP47 modulate DNA repair by controlling cellular levels of DNA polymerase β, and also that polynucleotide kinase phosphatase levels are controlled by ATM-dependant phosphorylation and Cul4A-DDB1-STRAP-dependent ubiquitylation.
Copy-number gains of HUWE1 due to replication- and recombination-based rearrangements.
Marynen et al., Leuven, Belgium. In Am J Hum Genet, 2012
Increased dosage of HUWE1 causes nonsyndromic intellectual disability.
HUWE1 ubiquitinates MyoD and targets it for proteasomal degradation.
Ciechanover et al., Haifa, Israel. In Biochem Biophys Res Commun, 2012
the involvement of HUWE1 in the ubiquitination and proteasomal degradation of MyoD was described.
The E3 ubiquitin ligase Mule acts through the ATM-p53 axis to maintain B lymphocyte homeostasis.
Mak et al., Toronto, Canada. In J Exp Med, 2012
Mule regulates the ATM-p53 axis to maintain B cell homeostasis under both steady-state and stress conditions.
Regulation of oxidative DNA damage repair by DNA polymerase λ and MutYH by cross-talk of phosphorylation and ubiquitination.
Hübscher et al., Zürich, Switzerland. In Proc Natl Acad Sci U S A, 2012
The E3 ligase Mule mediates the degradation of Pol lambda and the control of Pol lambda levels by Mule has functional consequences for the ability of mammalian cells to deal with 8-oxo-G lesions.
The double life of MULE in preeclamptic and IUGR placentae.
Caniggia et al., Toronto, Canada. In Cell Death Dis, 2011
In PE, MULE preferentially targeted p53 for degradation, allowing accumulation of pro-apoptotic Mcl-1 isoforms. In IUGR, however, MULE targeted pro-survival Mcl-1, allowing p53 to accumulate and exert its apoptotic function.
The emerging role of Mule and ARF in the regulation of base excision repair.
Dianov et al., Oxford, United Kingdom. In Febs Lett, 2011
Studies indicate that ARF is induced in response to DNA damage and inhibits, by direct interaction, the E3 ubiquitin ligase Mule.
The HECT-domain ubiquitin ligase Huwe1 controls neural differentiation and proliferation by destabilizing the N-Myc oncoprotein.
Lasorella et al., New York City, United States. In Nat Cell Biol, 2008
Huwe1 links destruction of N-Myc to the quiescent state that complements differentiation in the neural tissue
The ubiquitin ligase HectH9 regulates transcriptional activation by Myc and is essential for tumor cell proliferation.
Eilers et al., Marburg an der Lahn, Germany. In Cell, 2005
HectH9-mediated ubiquitination of Myc is required for transactivation of multiple target genes.
ARF-BP1/Mule is a critical mediator of the ARF tumor suppressor.
Gu et al., New York City, United States. In Cell, 2005
study modifies the current view of ARF-mediated p53 activation and reveals that ARF-BP1 is a critical mediator of both the p53-independent and p53-dependent tumor suppressor functions of ARF [ARF-BP1]
Mule/ARF-BP1, a BH3-only E3 ubiquitin ligase, catalyzes the polyubiquitination of Mcl-1 and regulates apoptosis.
Wang et al., Dallas, United States. In Cell, 2005
Mule is both required and sufficient for the polyubiquitination of Mcl-1; Mule is a unique BH3-containing E3 ubiquitin ligase apical to Bcl-2 family proteins during DNA damage-induced apoptosis
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