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17 documents found
1: Title: Melatonin-mediated downregulation of ZNF746 suppresses bladder tumorigenesis mainly through inhibiting the AKT-MMP-9 signaling pathway.
Authors: Chen, Yen-Ta, et.al. .
Journal: Journal of pineal research (J Pineal Res), Vol. 66 (1): e12536, 2019 .
Snippet: Transfection of T24 cells with plasmid-based shRNA (ie, ZNF746-silencing) downregulated the protein expression of MMP-9, cell growth, and invasion and attachment to endothelial cells but upregulated the colony formation (all P < 0.001).
Affiliation: Division of Urology, Department of Surgery, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan. Division of Nephrology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan. Department of Nursing, Asia University, Taichung, Taiwan. Division of Cardiology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan. Institute for Translational Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan. Center for Shockwave Medicine and Tissue Engineering, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan. Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, Taiwan. .
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2: Title: Zinc finger protein 746 promotes colorectal cancer progression via c-Myc stability mediated by glycogen synthase kinase 3β and F-box and WD repeat domain-containing 7.
Authors: Jung, Ji Hoon, et.al. .
Journal: Oncogene, Vol. 37 (27): 3715-3728, 2018 .
Snippet: Conversely, ZNF746 depletion attenuated phosphorylation of c-Myc (S62) and glycogen synthase kinase 3β (GSK3β) (S9) and also activated p-c-Myc (T58), which was reversed by GSK3 inhibitors such as SB-216763 and Enza.
Affiliation: Korean Medicine Tumor Ecosystem Regulation Research Center, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea. University Hospital Newark, NJ University Hospital 150 Bergen St, Newark, NJ, 07103, USA. Department of Otorhinolaryngology-Head and Neck Surgery, School of Medicine Kyung Hee University, Seoul, Republic of Korea. Department of Biomedical Sciences and Cancer Biology Center, Texas Tech University Health Sciences Center, Amarillo, TX, 79106, USA. Department of Otorhinolaryngology-Head and Neck Surgery, School of Medicine Kyung Hee University, Seoul, Republic of Korea. myyun91@khu.ac.kr. Korean Medicine Tumor Ecosystem Regulation Research Center, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea. sungkim7@khu.ac.kr. .
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3: Title: Plasma vascular non-inflammatory molecule 3 is associated with gastrointestinal acute graft-versus-host disease in mice.
Authors: Wang, Na, et.al. .
Journal: Journal of inflammation (London, England) (J Inflamm (lond)), Vol. 15, 2018 .
Snippet: These 5 proteins were VNN3, ZNF746, C4BP, KNG1 and FETUB, and they were consistent with results from negative labeling with 8-plex iTRAQ.
Affiliation: Wenzhou Medical University, Wenzhou, Zhejiang 325002 China. Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, 300020 China. Department of Hematology, The First Affiliated Hospital of Wenzhou Medical University, Nan Bai Xiang Street, Ouhai District, Wenzhou, Zhejiang 325002 China. .
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4: Title: PARIS reprograms glucose metabolism by HIF-1α induction in dopaminergic neurodegeneration.
Authors: Kang, Hojin, et.al. .
Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun), Vol. 495 (4): 2498-2504, 2018 .
Snippet: Our previous study found that PARIS (ZNF746) transcriptionally suppressed transketolase (TKT), a key enzyme in pentose phosphate pathway (PPP) in the substantia nigra (SN) of AAV-PARIS injected mice.
Affiliation: Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, South Korea. Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, South Korea; Samsung Medical Center (SMC), Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, South Korea. HuGeX Co., Ltd. Seongnam, 462-122, South Korea. Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, South Korea; Samsung Medical Center (SMC), Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, South Korea. Electronic address: jshin24@skku.edu. .
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5: Title: Identification of transketolase as a target of PARIS in substantia nigra.
Authors: Kim, Hyein, et.al. .
Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun), 2017 .
Snippet: Recently, PARIS (ZNF746) is introduced as authentic substrate of parkin and transcriptionally represses PGC-1α by binding to insulin responsive sequences (IRSs) in the promoter of PGC-1α.
Affiliation: Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, South Korea; HuGeX Co., Ltd., Seongnam 462-122, South Korea. Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, South Korea. Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, South Korea; Samsung Medical Center (SMC), Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, South Korea. HuGeX Co., Ltd., Seongnam 462-122, South Korea. Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, South Korea; Samsung Medical Center (SMC), Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, South Korea. Electronic address: jshin24@skku.edu. .
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6: Title: PINK1 Primes Parkin-Mediated Ubiquitination of PARIS in Dopaminergic Neuronal Survival.
Authors: Lee, Yunjong, et.al. .
Journal: Cell reports (Cell Rep), Vol. 18 (4): 918-932, 2017 .
Snippet: Parkin inactivation leads to accumulation of the parkin interacting substrate (PARIS, ZNF746) that plays an important role in dopamine cell loss through repression of proliferator-activated receptor gamma coactivator-1-alpha (PGC-1α) promoter activity.
Affiliation: Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, South Korea. Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685, USA; Diana Helis Henry Medical Research Foundation, New Orleans, LA 70130-2685, USA. Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, South Korea. Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685, USA. Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Department of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA; Mayo Graduate School, Neurobiology of Disease, Mayo Clinic, Jacksonville, FL 32224, USA. Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685, USA; Diana Helis Henry Medical Research Foundation, New Orleans, LA 70130-2685, USA. Electronic address: vdawson@jhmi.edu. Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, South Korea. Electronic address: jshin24@skku.edu. Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685, USA; Diana Helis Henry Medical Research Foundation, New Orleans, LA 70130-2685, USA. Electronic address: tdawson@jhmi.edu. .
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7: Title: SUMOylation of the KRAB zinc-finger transcription factor PARIS/ZNF746 regulates its transcriptional activity.
Authors: Nishida, Tamotsu, et.al. .
Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun), Vol. 473 (4): 1261-7, 2016 .
Snippet: Parkin-interacting substrate (PARIS), a member of the family of Krüppel-associated box (KRAB)-containing zinc-finger transcription factors, is a substrate of the ubiquitin E3 ligase parkin.
Affiliation: Department of Human Functional Genomics, Life Science Research Center, Mie University, 1577 Kurima-machiya, Tsu, Mie 514-8507, Japan. Electronic address: nishida@gene.mie-u.ac.jp. Department of Human Functional Genomics, Life Science Research Center, Mie University, 1577 Kurima-machiya, Tsu, Mie 514-8507, Japan. .
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8: Title: Potential Biomarkers of the Earliest Clinical Stages of Parkinson's Disease.
Authors: Alieva, Anelya Kh, et.al. .
Journal: Parkinson's disease (Parkinsons Dis), Vol. 2015, 2015 .
Snippet: An analysis of the mRNA levels of ATP13A2, PARK2, PARK7, PINK1, LRRK2, SNCA, ALDH1A1, PDHB, PPARGC1A, and ZNF746 genes in the peripheral blood of patients was carried out using reverse transcription followed by real-time PCR.
Affiliation: Institute of Molecular Genetics, Russian Academy of Sciences, Moscow 123182, Russia. Research Centre of Neurology, Moscow 125367, Russia. .
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9: Title: Mitochondrial Quality Control via the PGC1α-TFEB Signaling Pathway Is Compromised by Parkin Q311X Mutation But Independently Restored by Rapamycin.
Authors: Siddiqui, Almas, et.al. .
Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience (J Neurosci), Vol. 35 (37): 12833-44, 2015 .
Snippet: UNLABELLED: Following its activation by PINK1, parkin is recruited to depolarized mitochondria where it ubiquitinates outer mitochondrial membrane proteins, initiating lysosomal-mediated degradation of these organelles.
Affiliation: Buck Institute for Research on Aging, Novato, California 94945. Buck Institute for Research on Aging, Novato, California 94945 jandersen@buckinstitute.org. .
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10: Title: Parkin loss leads to PARIS-dependent declines in mitochondrial mass and respiration.
Authors: Stevens, Daniel A, et.al. .
Journal: Proceedings of the National Academy of Sciences of the United States of America (Proc Natl Acad Sci U S A), Vol. 112 (37): 11696-701, 2015 .
Snippet: Mutations in parkin lead to early-onset autosomal recessive Parkinson's disease (PD) and inactivation of parkin is thought to contribute to sporadic PD. Adult knockout of parkin in the ventral midbrain of mice leads to an age-dependent loss of dopamine neurons that is dependent on the accumulation of parkin interacting substrate (PARIS), zinc finger protein 746 (ZNF746), and its transcriptional repression of PGC-1α.
Affiliation: Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Solomon H. Snyder Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685; Diana Helis Henry Medical Research Foundation, New Orleans, LA 70130-2685; Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685; Diana Helis Henry Medical Research Foundation, New Orleans, LA 70130-2685; Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 446-746, South Korea; Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Department of Physiology, Ajou University School of Medicine, Suwon 443-721, Korea; Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Age-Related and Brain Disease Research Center, Department of Neuroscience, Kyung Hee University, Seoul, 130-701, South Korea; Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Well Aging Research Center, Samsung Advanced Institute of Technology, Yongin-si 446-712, Korea; Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685; Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685; Diana Helis Henry Medical Research Foundation, New Orleans, LA 70130-2685; Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Solomon H. Snyder Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685; Diana Helis Henry Medical Research Foundation, New Orleans, LA 70130-2685; Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Department of Physiology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 446-746, South Korea; tdawson@jhmi.edu jshin24@skku.edu. Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Solomon H. Snyder Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685; Diana Helis Henry Medical Research Foundation, New Orleans, LA 70130-2685; Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205; Department of Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD 21205 tdawson@jhmi.edu jshin24@skku.edu. .
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11: Title: Dysregulation of parkin in the substantia nigra of db/db and high-fat diet mice.
Authors: Khang, R, et.al. .
Journal: Neuroscience, Vol. 294, 2015 .
Snippet: Taken together, our data suggest that the dysregulation of Parkin-PARIS-PGC-1α pathway by metabolic malregulation may contribute to the pathogenesis of PD and metformin might exert a neuroprotective effect on PD via the restoration of parkin.
Affiliation: Division of Pharmacology, Department of Molecular Cell Biology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea. Division of Biochemistry and Molecular Biology, Department of Molecular Cell Biology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea; Mass Spectrometry, Research Core Facility, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea. Division of Pharmacology, Department of Molecular Cell Biology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea; Mass Spectrometry, Research Core Facility, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea. Electronic address: jshin24@skku.edu. .
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12: Title: Repression of rRNA transcription by PARIS contributes to Parkinson's disease.
Authors: Kang, Hojin, et.al. .
Journal: Neurobiology of disease (Neurobiol Dis), Vol. 73, 2015 .
Snippet: We previously demonstrated that PARIS (PARkin Interacting Substrate, ZNF746) transcriptionally suppresses peroxisome proliferator-activated receptor gamma (PPARγ) coactivator-1α (PGC-1α) in PD and its accumulation results in selective dopaminergic neuronal death.
Affiliation: Division of Pharmacology, Department of Molecular Cell Biology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Gyeonggi-do 440-746, Republic of Korea. Division of Pharmacology, Department of Molecular Cell Biology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Gyeonggi-do 440-746, Republic of Korea; Mass Spectrometry, Research Core Facility, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Gyeonggi-do 440-746, Republic of Korea. Electronic address: jshin24@skku.edu. .
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13: Title: Parkin-mediated ubiquitination of mutant glucocerebrosidase leads to competition with its substrates PARIS and ARTS.
Authors: Bendikov-Bar, Inna, et.al. .
Journal: Orphanet journal of rare diseases (Orphanet J Rare Dis), Vol. 9, 2014 .
Snippet: BACKGROUND: Parkinson's disease (PD) is a movement neurodegenerative disorder characterized by death of dopaminergic neurons in the substantia nigra pars compacta of the brain that leads to movement impairments including bradykinesia, resting tremor, postural instability and rigidity.
Affiliation: Department of Cell Research and Immunology, Life Sciences, Tel Aviv University, Levanon St, Ramat Aviv 69978, Israel. horwitzm@post.tau.ac.il. .
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14: Title: Inhibition of ZNF746 suppresses invasion and epithelial to mesenchymal transition in H460 non-small cell lung cancer cells.
Authors: Kim, Bonglee, et.al. .
Journal: Oncology reports (Oncol Rep), Vol. 31 (1): 73-8, 2014 .
Snippet: Although ZNF746, also known as Parkin-interacting substrate (PARIS), has been reported to suppress peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and its target gene NRF-1 leading to the neurodegeneration in Parkinson's disease, its function in tumorigenesis has yet to be investigated.
Affiliation: College of Oriental Medicine, Kyung Hee University, Dongdaemun-gu, Seoul 130-701, Republic of Korea. .
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15: Title: Parkin plays a role in sporadic Parkinson's disease.
Authors: Dawson, Ted M, et.al. .
Journal: Neuro-degenerative diseases (Neurodegener Dis), Vol. 13 (2-3): 69-71, 2014 .
Snippet: RESULTS: Parkin is inactivated in sporadic PD via S-nitrosylation, oxidative and dopaminergic stress, and phosphorylation by the stress-activated kinase c-Abl, leading to the accumulation of AIMP2 and PARIS (ZNF746).
Affiliation: Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, Md., USA. .
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16: Title: Parkin inactivation via PARIS (ZNF746) may lead to neurodegeneration in Parkinson's disease.
Journal: Movement disorders : official journal of the Movement Disorder Society (Mov Disord), Vol. 26 (5): 772, 2011 .
No Abstract available.
Affiliation: Clinical Ageing Research Unit, Institute for Ageing & Health Newcastle University, Newcastle-upon-Tyne, United Kingdom. .
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17: Title: PARIS (ZNF746) repression of PGC-1α contributes to neurodegeneration in Parkinson's disease.
Authors: Shin, Joo-Ho, et.al. .
Journal: Cell, Vol. 144 (5): 689-702, 2011 .
Snippet: Here, we identify a new parkin interacting substrate, PARIS (ZNF746), whose levels are regulated by the ubiquitin proteasome system via binding to and ubiquitination by the E3 ubiquitin ligase, parkin.
Affiliation: NeuroRegeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. .
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