Ascending Colon Cancer with Hepatic Metastasis and Cholecystolithiasis in a Patient with Situs Inversus Totalis Without Any Expression of UVRAG mRNA: Report of a Case

Goi, Takanori; Kawasaki, Motomi; Yamazaki, Tomoo; Kono, Kenji; Katayama, Kanji; Hirose, Kazuo; Yamaguchi, Akio

doi:10.1007/s00595-002-2567-y

Cited by 53 publications

(43 citation statements)

References 10 publications

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“…146 Mutation of UVRAG is frequently observed in various human cancers and may be responsible for the etiology of these cancers. [147][148][149][150] UVRAG is critical for DNA repair and chromosomal stability, especially in response to radiation. [151][152][153] Using GST affinity isolation, UVRAG was identified as a binding partner of BECN1-PIK3C3, which directly interacts with BECN1 via its CCD.…”

Section: Regulation Of Autophagy By Pik3c3 Via Atg14mentioning

confidence: 99%

Differential regulatory functions of three classes of phosphatidylinositol and phosphoinositide 3-kinases in autophagy

2015

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Abbreviations: 3-MA, 3-methyladenine; AMBRA1, autophagy/Beclin 1 regulator 1; ATG, autophagy related; ATM, ATM serine/threonine kinase; ATR, ATR serine/threonine kinase; BH3, Bcl-2 homology 3; CCD, coiled-coil domain; CDK, cyclin-dependent kinase; CISD2, CDGSH iron sulfur domain 2; class I/II PI3K, class I/II phosphoinositide 3-kinase; class III PtdIns3K, class III phosphatidylinositol 3-kinase; DAPK1, death-associated protein kinase 1; DDR, DNA damage response; EIF4EBP1, eukaryotic translation initiation factor 4E binding protein 1; ER, endoplasmic reticulum; FOXO, forkhead box O; FYCO1, FYVE and coiledcoil domain containing 1; GAP, GTPase-activating protein; HMGB1, high mobility group box 1; HSPA1A, heat shock 70kDa protein 1A; IR, ionizing radiation; MAPK8, mitogen-activated protein kinase 8; MEFs, mouse embryonic fibroblasts; MTMR, myotubularin-related protein; MTOR, mechanistic target of rapamycin (serine/threonine kinase); MTORC1, mechanistic target of rapamycin complex 1; MVBs, spherical multivesicular bodies; NRBF2, nuclear receptor binding factor 2; PAS, phagophore assembly site; PDPK1, 3-phosphoinositide dependent protein kinase 1; PE, phosphatidylethanolamine; PIKFYVE, phosphoinositide kinase, FYVE finger containing; PINK1, PTEN-induced putative kinase 1; PtdIns3K-C1, class III phosphatidylinositol 3-kinase complex I; PtdIns3K-C2, class III phosphatidylinositol 3-kinase complex II; PKB, protein kinase B; PRKA, protein kinase, AMP-activated; PRKD1, protein kinase D1; PRKDC, protein kinase, DNA-activated, catalytic polypeptide; PtdIns5P, phosphatidylinositol 5-phosphate; PtdIns4P, phosphatidylinositol 4-phosphate; PtdIns(4,5)P 2 , phosphatidylinositol 4,5-bisphosphate; PtdIns3P, phosphatidylinositol 3-phosphate; PtdIns(3,5)P 2 , phosphatidylinositol 3,5-bisphosphate; PtdIns(3,4,5)P 3 , phosphatidylinositol 3,4,5-trisphosphate; RHEB, Ras homolog enriched in brain; RPS6KB1, ribosomal protein S6 kinase, 70kDa, polypeptide 1; SQSTM1, sequestosome 1; TECPR1, tectonin b-propeller repeat containing 1; TFEB, transcription factor EB; TRIM28, tripartite motif containing 28; TSC, tuberous sclerosis; UV, ultraviolet; UVRAG, UV radiation resistance associated; WDFY3, WD repeat and FYVE domain containing 3; WIPI, WD repeat domain, phosphoinositide interacting; ZFYVE1, zinc finger, FYVE domain containing 1.Autophagy is an evolutionarily conserved and exquisitely regulated self-eating cellular process with important biological functions. Phosphatidylinositol 3-kinases (PtdIns3Ks) and phosphoinositide 3-kinases (PI3Ks) are involved in the autophagic process. Here we aim to recapitulate how 3 classes of these lipid kinases differentially regulate autophagy. Generally, activation of the class I PI3K suppresses autophagy, via the well-established PI3K-AKT-MTOR (mechanistic target of rapamycin) complex 1 (MTORC1) pathway. In contrast, the class III PtdIns3K catalytic subunit PIK3C3/Vps34 forms a protein complex with BECN1 and PIK3R4 and produces phosphatidylinositol 3-phosphate (PtdIns3P), which is required for the initiati...

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Section: Regulation Of Autophagy By Pik3c3 Via Atg14mentioning

confidence: 99%

Differential regulatory functions of three classes of phosphatidylinositol and phosphoinositide 3-kinases in autophagy

2015

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“…It maps to a tumor-susceptibility locus on human chromosome 11q13 that is frequently implicated in common human cancers, including breast, colorectal and gastric cancers. [15][16][17][18] UVRAG consists of four major regions: the proline-rich (PR) domain (residues 1-41), the calcium-dependent lipid-binding C2 domain (residues 42-147), the coiled-coil domain (CCD, residues 200-269) and a C-terminal domain (residues 270-699) presumed to be unstructured (Fig. 1A).…”

Section: Uvrag In Briefmentioning

confidence: 99%

Beyond autophagy: The role of UVRAG in membrane trafficking

Liang¹,

Sir²,

Lee³

et al. 2008

Autophagy

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“…[11][12][13][14] Interestingly, as seen with Beclin 1, UVRAG is monoallelically mutated in various human colon cancer cells and tissues, suggesting that UVRAG is a tumor suppressor candidate. We also demonstrate that recovery of UVRAG expression in autophagy-defective human HCT116 colon cancer cells that carry a monoallelic mutation in the UVRAG gene leads to the extensive accumulation of autophagosomes, whereas RNAi-mediated knockdown of UVRAG in autophagy-competent cells prevents the accretion of autophagosomes.…”

mentioning

confidence: 99%