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

Ubiquitin specific peptidase 6

TRE2, USP6, TRE17, HRP-1
Top mentioned proteins: ACID, TBC, CAN, Rab5, Ubiquitin
Papers using TRE2 antibodies
Impaired mammary gland and lymphoid development caused by inducible expression of Axin in transgenic mice
Costantini Frank et al., In The Journal of Cell Biology, 1998
... 6.4-kb NheI-EcoRV fragment of MT–Axin–IRES2–GFP–hβG3′ was then inserted into the same restriction sites downstream of TRE2, which consisted of seven copies of the tet operator and a minimal CMV promoter (CLONTECH Laboratories, Inc.).
Papers on TRE2
The evolutionarily conserved Tre2/Bub2/Cdc16 (TBC), Lysin motif (LysM), Domain catalytic (TLDc) domain is neuroprotective against oxidative stress.
Oliver et al., Oxford, United Kingdom. In J Biol Chem, Jan 2016
OXR1 contains the Tre2/Bub2/Cdc16 (TBC), Lysin motif (LysM), Domain catalytic (TLDC) domain, a motif present in a family of proteins including TBC1 domain family member 24 (TBC1D24), a protein mutated in a range of disorders characterized by seizures, hearing loss and neurodegeneration.
The integration of autophagy and cellular trafficking pathways via RAB GAPs.
Behl et al., Mainz, Germany. In Autophagy, Nov 2015
A role in macroautophagy regulation for different TRE2-BUB2-CDC16 (TBC) domain-containing RAB GAPs has been established.
Soft-tissue aneurysmal bone cyst with translocation t(17;17)(p13;q21) corresponding to COL1A1 and USP6 loci.
Horvai et al., San Francisco, United States. In Skeletal Radiol, Nov 2015
This diagnosis was supported by cytogenetic analysis revealing a t(17;17)(p13;q21) translocation corresponding to the USP6 and COL1A1 loci.
APOE Isoforms Control Pathogenic Subretinal Inflammation in Age-Related Macular Degeneration.
Sennlaub et al., Paris, France. In J Neurosci, Nov 2015
We here show using targeted replacement mice expressing the human APOE isoforms (TRE2, TRE3, and TRE4) that MPs of TRE2 mice express increased levels of APOE, interleukin-6, and CCL2 and develop subretinal MP accumulation, photoreceptor degeneration, and exaggerated choroidal neovascularization similar to AMD.
Regulation of mTORC1 by PI3K signaling.
Cantley et al., Boston, United States. In Trends Cell Biol, Sep 2015
We focus on how PI3K-dependent activation of Akt and spatial regulation of the tuberous sclerosis complex (TSC) complex (TSC complex) [composed of TSC1, TSC2, and Tre2-Bub2-Cdc16-1 domain family member 7 (TBC1D7)] switches on Rheb at the lysosome, where mTORC1 is activated.
PT-1 selectively activates AMPK-γ1 complexes in mouse skeletal muscle, but activates all three γ subunit complexes in cultured human cells by inhibiting the respiratory chain.
Richter et al., Copenhagen, Denmark. In Biochem J, Jun 2015
PT-1 increased the AMPK-dependent phosphorylation of the autophagy-regulating kinase ULK1 (unc-51-like autophagy-activating kinase 1) on Ser555, but not proposed AMPK-γ3 substrates such as Ser231 on TBC1 (tre-2/USP6, BUB2, cdc16) domain family, member 1 (TBC1D1) or Ser212 on acetyl-CoA carboxylase subunit 2 (ACC2), nor did it stimulate glucose transport.
AMPKα is critical for enhancing skeletal muscle fatty acid utilization during in vivo exercise in mice.
Wojtaszewski et al., Copenhagen, Denmark. In Faseb J, May 2015
A decreased muscle protein expression of CD36 (cluster of differentiation 36) and FABPpm (plasma membrane fatty acid binding protein) (by ∼17-40%), together with fully abolished TBC1D1 (tre-2/USP6, BUB2, cdc16 domain family member 1) Ser(237) phosphorylation during contraction/exercise in AMPKα mdKO mice, may impair FA transport capacity and FA transport protein translocation to sarcolemma, respectively.
A spontaneously resolving breast lesion: imaging and cytological findings of nodular fasciitis of the breast with FISH showing USP6 gene rearrangement.
Bourke et al., Australia. In Bmj Case Rep, 2014
The cytological features in conjunction with immunohistochemistry and the clinical history strongly suggest nodular fasciitis, which is further supported by a USP6 FISH positive result.
Secondary aneurysmal bone cyst in the distal humerus after resection of intra-articular nodular fasciitis of the elbow.
Hirata et al., Nagoya, Japan. In Bmc Res Notes, 2014
The findings of this case suggest that these two tumors reside in the same biologic spectrum defined as USP6-induced tumors.
Secondary jaw aneurysmal bone cyst (JABC)--a possible misnomer? A review of literature on secondary JABCs, their pathogenesis and oncogenesis.
Kapoor et al., In J Oral Pathol Med, 2014
The search for histopathogenesis pointed to a specific cytogenetic abnormality as the origin of primary ABCs, with USP6 as its main oncogene and spindle cell as the neoplastic cell, unlike with secondary ABCs, suggesting that they are distinct pathological processes.
Disruption of O-GlcNAc Cycling in C. elegans Perturbs Nucleotide Sugar Pools and Complex Glycans.
Hanover et al., Bethesda, United States. In Front Endocrinol (lausanne), 2013
Transcripts of genes encoding for key members in the HBP (gfat-2, gna-2, C36A4.4) and trehalose metabolism (tre-1, tre-2, tps-2) were elevated in ogt-1 null animals.
The TBC1D1 gene: structure, function, and association with obesity and related traits.
Bertolini et al., Bologna, Italy. In Vitam Horm, 2012
This review summarizes what is currently known on the TBC1 (tre-2/USP6, BUB2, cdc16) domain family, member 1 (TBC1D1) gene and gives an overview of its links with human obesity and related traits, taking also information from other animals.
Illuminating the functional and structural repertoire of human TBC/RABGAPs.
Braga et al., London, United Kingdom. In Nat Rev Mol Cell Biol, 2012
The Tre2-Bub2-Cdc16 (TBC) domain-containing RAB-specific GTPase-activating proteins (TBC/RABGAPs) are characterized by the presence of highly conserved TBC domains and act as negative regulators of RABs.
The oncogenic TBC domain protein USP6/TRE17 regulates cell migration and cytokinesis.
Haucke et al., Berlin, Germany. In Biol Cell, 2012
manipulating USP6 expression levels alters the ability of cells to migrate and to divide. Cell proliferation and progression through cytokinesis depend on USP6 expression
TRE17/USP6 oncogene translocated in aneurysmal bone cyst induces matrix metalloproteinase production via activation of NF-kappaB.
Chou et al., Philadelphia, United States. In Oncogene, 2010
TRE17 is sufficient to initiate tumorigenesis, identify MMPs as novel TRE17 effectors that likely contribute to aneurysmal bone cyst pathogenesis.
Frequency of USP6 rearrangements in myositis ossificans, brown tumor, and cherubism: molecular cytogenetic evidence that a subset of "myositis ossificans-like lesions" are the early phases in the formation of soft-tissue aneurysmal bone cyst.
Oliveira et al., Rochester, United States. In Skeletal Radiol, 2008
No USP6 rearrangements were found in cherubism or brown tumors. USP6 rearrangements were identified in 2 patients with myositis ossificans.
Mutational analysis of the TRE2 oncogene encoding an inactive RabGAP.
Vandenbol et al., Gembloux, Belgium. In Biotechnol Lett, 2007
The lack of secondary structure of the region flanking the TBC domain in TRE2 may explain why this region plays a role in the lack of GAP activity, even when a potentially functional TBC domain is present.
Calcium/calmodulin regulates ubiquitination of the ubiquitin-specific protease TRE17/USP6.
Chou et al., Philadelphia, United States. In J Biol Chem, 2005
Ca2+/CaM has a role in regulating ubiquitination through direct interaction with TRE17
Long lifespan in worms with long telomeric DNA.
Lee et al., Seoul, South Korea. In Nat Genet, 2004
We examined the effect of telomere length on lifespan by overexpressing HRP-1, a telomere-binding protein, which gradually increased telomere length in worms.
The yeast DOA4 gene encodes a deubiquitinating enzyme related to a product of the human tre-2 oncogene.
Hochstrasser et al., Chicago, United States. In Nature, 1993
The human tre-2 oncogene encodes a deubiquitinating enzyme similar to Doa4, indicating a role for the ubiquitin system in mammalian growth control.
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