Article
Plant Sciences
Xiao-Qing Yang, Wei Li, Zhong-Ying Ren, Jun-Jie Zhao, Xin-Yang Li, Xing-Xing Wang, Xiao-Yu Pei, Yan-Gai Liu, Kun-Lun He, Fei Zhang, Xiong-Feng Ma, Dai-Gang Yang
Summary: This study identified GhSINA1 as a negative regulator in cotton fiber development through its interaction with itself and other GhSINA1 proteins, forming homodimers and heterodimers.
PLANT PHYSIOLOGY AND BIOCHEMISTRY
(2023)
Article
Plant Sciences
Zhongying Ren, Wei Liu, Xingxing Wang, Mingjiang Chen, Junjie Zhao, Fei Zhang, Hongjie Feng, Ji Liu, Daigang Yang, Xiongfeng Ma, Wei Li
Summary: Ubiquitination is a post-translational regulatory mechanism in plants, and the SEVEN IN ABSENTIA (SINA) ubiquitin ligases in upland cotton have been identified as positive regulators of defense responses against Verticillium dahliae.
FRONTIERS IN PLANT SCIENCE
(2021)
Review
Biochemistry & Molecular Biology
Olga Buneeva, Alexei Medvedev
Summary: Ubiquitination is a major post-translational modification of proteins, and atypical ubiquitination plays a crucial role in the development of Parkinson's disease, targeting proteins involved in the disease mechanism.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Biochemistry & Molecular Biology
Poyu Chen, Nancy De Winne, Geert De Jaeger, Masaki Ito, Maren Heese, Arp Schnittger
Summary: In Arabidopsis thaliana, the activity of the Bloom syndrome complex, which is crucial for maintaining genome integrity, is controlled by selective autophagy. The DNA damage regulator KNO1 facilitates autophagic degradation of RMI1, a structural component of the complex, leading to increased homologous recombination. Reduced autophagic activity makes plants hypersensitive to DNA damage. KNO1 itself is stabilized by the ubiquitin-proteasome system upon DNA damage, mediated by UBP12 and UBP13 deubiquitinases. These findings reveal a regulatory cascade of interconnected protein degradation steps that fine-tune the homologous recombination response to DNA damage.
Article
Biochemistry & Molecular Biology
Yu-Ling Hsu, Huey-Shan Hung, Chia-Wen Tsai, Shih-Ping Liu, Yu-Ting Chiang, Yun-Hua Kuo, Woei-Cherng Shyu, Shinn-Zong Lin, Ru-Huei Fu
Summary: Parkinson's disease is a degenerative disease that causes motor, cognitive, and behavioral disorders. The extract peiminine from Fritillaria thunbergii Miq has antioxidant and anti-neuroinflammatory effects, showing neuroprotective potential in PD models by reducing oxidative stress and cell degeneration and enhancing autophagy. Additionally, peiminine reduces the accumulation of alpha-synuclein, suggesting it as a promising candidate for further evaluation in PD treatment.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Pharmacology & Pharmacy
Zhifei Xu, Wentong Wu, Hao Yan, Yuhuai Hu, Qiaojun He, Peihua Luo
Summary: The tumor suppressor protein p53 plays a crucial role in controlling key biological functions and its mutation is associated with various diseases. Regulation of p53 stability is important for maintaining normal functions and targeting p53 for degradation could be a potential therapeutic strategy against cancer.
BIOCHEMICAL PHARMACOLOGY
(2021)
Review
Biochemistry & Molecular Biology
Ga Hyun Park, Joon Hyung Park, Kwang Chul Chung
Summary: Parkinson's disease is caused by the loss of dopaminergic neurons due to mitochondrial dysfunction, leading to toxic oligomer formation of alpha-synuclein. Familial PD-related proteins such as alpha-synuclein play a role in mitophagy, with defective changes in mitochondrial dynamics inducing the formation of toxic protein aggregates in PD. The genes involved in mitochondrial quality control and UPS are closely related to PD pathogenesis and may provide valuable therapeutic clues for management strategies.
Review
Cell Biology
Bipul Ray, Arehally M. Mahalakshmi, Sunanda Tuladhar, Abid Bhat, Asha Srinivasan, Christophe Pellegrino, Anbarasu Kannan, Srinivasa Rao Bolla, Saravana Babu Chidambaram, Meena Kishore Sakharkar
Summary: Parkinson's disease is characterized by the aggregation of α-synuclein protein, forming Lewy bodies, with several mutations in α-synuclein identified as potential causes. The spread of pathological α-synuclein between cells is believed to play a significant role in the development of the disease. It has been suggested that the pathology of Parkinson's disease may originate in the gastrointestinal tract and spread to the brain via the vagus nerve.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Immunology
Jia Lu, Chenfei Wang, Xin Cheng, Ruizhi Wang, Xuehan Yan, Pengju He, Hongzhuan Chen, Zhihua Yu
Summary: The study suggests that modulating microglial metabolism and activating TRPV1 channels may be a promising therapeutic strategy for Parkinson's disease, as they can improve energy metabolism and attenuate neurodegeneration.
JOURNAL OF NEUROINFLAMMATION
(2022)
Review
Biochemistry & Molecular Biology
Maria Dolores Perez-Carrion, Inmaculada Posadas, Javier Solera, Valentin Cena
Summary: This review summarizes the main pathological mutations in LRRK2 that contribute to Parkinson's disease and discusses the different cellular and therapeutic strategies to correct LRRK2 homeostasis.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Cell Biology
Hai-Yue Tu, Bao-Shi Yuan, Xiao-Ou Hou, Xiao-Jun Zhang, Chong-Shuang Pei, Ya-Ting Ma, Ya-Ping Yang, Yi Fan, Zheng-Hong Qin, Chun-Feng Liu, Li-Fang Hu
Summary: The extracellular transfer of alpha-Synuclein (alpha-Syn) contributes to Parkinson's disease pathogenesis by activating microglia and neuroinflammation. This study found that extracellular alpha-Syn inhibits microglia autophagy through Toll-like receptor 4 (Tlr4)-mediated p38 and Akt-mTOR signaling pathways, leading to neuroinflammation and PD development.
Article
Behavioral Sciences
Jaquelini B. Canever, Ericks Sousa Soares, Nubia C. P. de Avelar, Helena I. Cimarosti
Summary: This review provides an overview of the pathophysiological roles of alpha-synuclein in Parkinson's disease and discusses various post-translational modifications that are implicated in its functions. It also highlights the potential of alpha-synuclein PTMs as biomarkers for PD.
BEHAVIOURAL BRAIN RESEARCH
(2023)
Review
Neurosciences
Fan Zhang, Zhiwei Wu, Fei Long, Jieqiong Tan, Ni Gong, Xiaorong Li, Changwei Lin
Summary: This article summarizes the effects of ATP13A2 gene mutations on PD, discusses the molecular mechanism of lysosomal autophagy inhibition and abnormal alpha-synuclein accumulation, and provides a new direction for future research on the pathogenesis and therapeutic targets of ATP13A2 gene-related PD.
FRONTIERS IN CELLULAR NEUROSCIENCE
(2022)
Review
Biochemistry & Molecular Biology
Lior Nechushtai, Dan Frenkel, Ronit Pinkas-Kramarski
Summary: This article reviews the role of autophagy in the pathogenesis of Parkinson's disease, highlighting the relationship between impaired autophagy and the neurotoxic accumulation of protein aggregates as well as the death of dopaminergic neurons and neuroinflammation.
Review
Biochemistry & Molecular Biology
Rubina Roy, Rajib Paul, Pallab Bhattacharya, Anupom Borah
Summary: Parkinson's disease is a neurodegenerative disease that causes dopamine depletion and motor deficits. Nanovesicle technology has advantages in delivering drugs to the target site, leading to improved therapeutic efficacy. Multiple drug-carrying abilities of nanovesicles have also shown success in targeting different pathological events of PD.
ACS CHEMICAL NEUROSCIENCE
(2023)
Article
Biochemistry & Molecular Biology
Hazem Safory, Samah Neame, Yoav Shulman, Salman Zubedat, Inna Radzishevsky, Dina Rosenberg, Hagit Sason, Simone Engelender, Avi Avital, Swen Huelsmann, Jackie Schiller, Herman Wolosker
Article
Biochemistry & Molecular Biology
Jingnan Liu, Tianxia Li, Joseph M. Thomas, Zhong Pei, Haibing Jiang, Simone Engelender, Christopher A. Ross, Wanli W. Smith
HUMAN MOLECULAR GENETICS
(2016)
Article
Biochemistry & Molecular Biology
Raymonde Szargel, Vered Shani, Fatimah Abd Elghani, Lucy N. Mekies, Esti Liani, Ruth Rott, Simone Engelender
HUMAN MOLECULAR GENETICS
(2016)
Article
Multidisciplinary Sciences
Frederick C. Nucifora, Leslie G. Nucifora, Chee-Hoe Ng, Nicolas Arbez, Yajuan Guo, Elaine Roby, Vered Shani, Simone Engelender, Dong Wei, Xiao-Fang Wang, Tianxia Li, Darren J. Moore, Olga Pletnikova, Juan C. Troncoso, Akira Sawa, Ted M. Dawson, Wanli Smith, Kah-Leong Lim, Christopher A. Ross
NATURE COMMUNICATIONS
(2016)
Article
Multidisciplinary Sciences
Ruth Rott, Raymonde Szargel, Vered Shani, Haya Hamza, Mor Savyon, Fatimah Abd Elghani, Rina Bandopadhyay, Simone Engelender
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2017)
Review
Neurosciences
Simone Engelender, Ole Isacson
TRENDS IN NEUROSCIENCES
(2017)
Article
Neurosciences
Adeline H. Basil, Joan P. L. Sim, Grace G. Y. Lim, Shuping Lin, Hui Ying Chan, Simone Engelender, Kah-Leong Lim
FRONTIERS IN CELLULAR NEUROSCIENCE
(2017)
Review
Immunology
Penelope J. Hallett, Simone Engelender, Ole Isacson
JOURNAL OF NEUROINFLAMMATION
(2019)
Article
Multidisciplinary Sciences
Samah Neame, Hazem Safory, Inna Radzishevsky, Ayelet Touitou, Francesco Marchesani, Marialaura Marchetti, Shai Kellner, Shai Berlin, Veronika N. Foltyn, Simone Engelender, Jean-Marie Billard, Herman Wolosker
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2019)
Article
Biochemistry & Molecular Biology
Vered Shani, Hazem Safory, Raymonde Szargel, Ninghan Wang, Tsipora Cohen, Fatimah Abd Elghani, Haya Hamza, Mor Savyon, Inna Radzishevsky, Lihi Shaulov, Ruth Rott, Kah-Leong Lim, Christopher A. Ross, Rina Bandopadhyay, Hui Zhang, Simone Engelender
HUMAN MOLECULAR GENETICS
(2019)
Letter
Clinical Neurology
Zagorka Vitic, Hazem Safory, Vukasin M. Jovanovic, Yael Sarusi, Alexandra Stavsky, Joy Kahn, Alona Kuzmina, Lilah Toker, Daniel Gitler, Ran Taube, Roland H. Friedel, Simone Engelender, Claude Brodski
Article
Biochemistry & Molecular Biology
Li Shu, Chao Hu, Meng Xu, Jianglong Yu, He He, Jie Lin, Hongying Sha, Bin Lu, Simone Engelender, Minxin Guan, Zhiyin Song
Summary: Mitochondrial DNA is susceptible to damage, especially under oxidative stress. A newly identified mitophagy receptor, ATAD3B, promotes the clearance of damaged mtDNA induced by oxidative stress. ATAD3B hetero-oligomerizes with ATAD3A under normal conditions, but oxidative stress-induced mtDNA damage disrupts this interaction and triggers mitophagy.
Article
Clinical Neurology
Simone Engelender, Leonidas Stefanis, Salvatore Oddo, Arianna Bellucci
Summary: Neurodegenerative proteinopathies are a class of neurodegenerative disorders characterized by the accumulation of abnormal protein deposits. Stimulating protein degradation pathways may be a potential therapeutic strategy, but there are gaps and controversies in both experimental and clinical studies.
MOVEMENT DISORDERS
(2022)
Article
Cell Biology
Fatimah Abd Elghani, Hazem Safory, Haya Hamza, Mor Savyon, Malik Farhoud, Michal Toren-Hershoviz, Zagorka Vitic, Kirsten Ebanks, Vered Shani, Sleman Bisharat, Lihi Shaulov, Claude Brodski, Zhiyin Song, Rina Bandopadhyay, Simone Engelender
Summary: Parkinson's disease (PD) is characterized by the degeneration of dopaminergic neurons in the substantia nigra. In PD, there is an accumulation of alpha-synuclein in Lewy bodies and dysfunctional mitochondria. This study found that SIAH3 protein is increased in the brains and cerebrospinal fluid of PD patients, as well as in neurons treated with alpha-synuclein. SIAH3 interacts with PINK1, leading to their aggregation in mitochondria and triggering toxicity, mitochondrial dysfunction, and neuronal death. The increase in SIAH3 and its aggregation with PINK1 may contribute to alpha-synuclein pathology and prevent the removal of dysfunctional mitochondria.
Article
Clinical Neurology
Hugo Vicente Miranda, Eva M. Szego, Luis M. A. Oliveira, Carlo Breda, Ekrem Darendelioglu, Rita M. de Oliveira, Diana G. Ferreira, Marcos A. Gomes, Ruth Rott, Marcia Oliveira, Francesca Munari, Francisco J. Enguita, Tania Simoes, Eva F. Rodrigues, Michael Heinrich, Ivo C. Martins, Irina Zamolo, Olaf Riess, Carlos Cordeiro, Ana Ponces-Freire, Hilal A. Lashuel, Nuno C. Santos, Luisa V. Lopes, Wei Xiang, Thomas M. Jovin, Deborah Penque, Simone Engelender, Markus Zweckstetter, Jochen Klucken, Flaviano Giorgini, Alexandre Quintas, Tiago F. Outeiro