Article
Biochemistry & Molecular Biology
Murali Vijayan, P. Hemachandra Reddy
Summary: The study aims to understand the protective effects of reduced VDAC1 on mitochondrial dynamics and biogenesis in transgenic TAU mice. The researchers found that a decrease in VDAC1 can significantly reduce mitochondrial fission proteins and increase mitochondrial fusion and biogenesis proteins. These findings may have significant implications for the development of reduced-VDAC1-based treatments for AD and tauopathies.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Biochemistry & Molecular Biology
Geer Tian, Junteng Zhou, Yue Quan, Qihang Kong, Junli Li, Yanguo Xin, Wenchao Wu, Xiaoqiang Tang, Xiaojing Liu
Summary: This study provides evidence that dysregulation of fatty acid oxidation contributes to fibroblast activation and cardiac fibrosis. Downregulation of fatty acid oxidation leads to the fibroblast-to-myofibroblast transition. VDAC1 plays a crucial role in maintaining fatty acid oxidation metabolism, and VDAC1 peptide shows potential as a drug for suppressing cardiac fibrosis.
Article
Physiology
Hirohito Shimizu, Simon Huber, Adam D. Langenbacher, Lauren Crisman, Jie Huang, Kevin Wang, Fabiola Wilting, Thomas Gudermann, Johann Schredelseker, Jau-Nian Chen
Summary: Mitochondrial VDAC proteins play a crucial role in regulating cardiac rhythmicity, with overexpression of VDAC1 and VDAC2 suppressing arrhythmia. The presence of glutamate at position 73 in VDAC1 and VDAC2, and glutamine in VDAC3, determines their isoform-specific functions in controlling Ca2+ transport. Mutation of E73 or Q73 affects the anti-arrhythmic effect of VDAC isoforms by modulating Ca2+ cross-talk between the sarcoplasmic reticulum and mitochondria in cardiomyocytes.
FRONTIERS IN PHYSIOLOGY
(2021)
Article
Cell Biology
Murali Vijayan, Rainier Vladlen Alvir, Razelle Vladlen Alvir, Lloyd E. Bunquin, Jangampalli Adi Pradeepkiran, P. Hemachandra Reddy
Summary: This study reveals the age-dependent increase of VDAC1 in Alzheimer's disease and its abnormal interaction with P-Tau, which results in mitochondrial defects. Partial reduction of VDAC1 in transgenic TAU mice reduces mitochondrial and synaptic toxicities and improves behavioral impairments.
Article
Biochemistry & Molecular Biology
Uttpal Anand, Anna Shteinfer-Kuzmine, Gal Sela, Manikandan Santhanam, Benjamin Gottschalk, Rajaa Boujemaa-Paterski, Ohad Medalia, Wolfgang F. Graier, Varda Shoshan-Barmatz
Summary: The mitochondrial protein VDAC1 plays a crucial role in regulating various cellular processes, including metabolism, apoptosis, and cell signaling. In this study, a short peptide derived from the N-terminal region of VDAC1 was designed to improve cellular stability and activity. The peptide exhibited multiple effects on cancer cells, such as apoptosis induction, autophagy, senescence, and cell adhesion. Furthermore, the peptide altered the expression of proteins associated with cell metabolism and signaling. These findings highlight the importance of VDAC1 in controlling diverse cellular functions through its interaction with other proteins.
Review
Cell Biology
Joyce T. Varughese, Susan K. Buchanan, Ashley S. Pitt
Summary: Voltage-dependent anion channel (VDAC) is a beta-barrel membrane protein located in the outer mitochondrial membrane, playing major roles in regulating various physiological processes and contributing to the development of diseases.
Review
Immunology
Yun Li, Xiaohuan Xia, Yi Wang, Jialin C. Zheng
Summary: This review summarizes the latest progress on the relationship between mitochondrial dysfunction and microglial activation in AD, highlighting the importance of studying this relationship and potential therapeutic strategies.
JOURNAL OF NEUROINFLAMMATION
(2022)
Review
Virology
Ahmed H. Saadawy, Aya M. Khalil, Lydia R. Sidarous, Mostafa S. Ibrahim, Tamer Z. Salem
Summary: Viruses control host cells by exploiting the molecular machinery to aid in viral replication and spread. Understanding viral mechanisms and biochemical pathways is essential for developing effective therapeutics against viral infections. The mitochondrion, particularly the voltage-dependent anion channel (VDAC) in the outer mitochondrial membrane, is targeted by many viruses. VDAC regulates metabolite flux, reactive oxygen species production, and apoptosis by releasing pro-apoptotic proteins. This review explores the role of VDAC in viral pathogenesis and its potential as an antiviral target through its interaction with viral proteins.
REVIEWS IN MEDICAL VIROLOGY
(2023)
Article
Neurosciences
Ankit Verma, Anna Shteinfer-Kuzmine, Nikita Kamenetsky, Srinivas Pittala, Avijit Paul, Edna Nahon Crystal, Alberto Ouro, Vered Chalifa-Caspi, Swaroop Kumar Pandey, Alon Monsengo, Noga Vardi, Shira Knafo, Varda Shoshan-Barmatz
Summary: Alzheimer's disease (AD) is associated with mitochondrial dysfunctions, and VDAC1 plays a key role in controlling metabolism and calcium homeostasis. This study used a newly developed inhibitor, VBIT-4, to target VDAC1 and prevent mitochondrial dysfunction and cell death.
TRANSLATIONAL NEURODEGENERATION
(2022)
Review
Cell Biology
Sagarika Banerjee, Rupesh Chaturvedi, Anu Singh, Hemant R. Kushwaha
Summary: This review article provides a consolidated summary of the research findings on hTid-1. It highlights the crucial role of hTid-1 in various cellular processes and diseases. The protein-protein interactions of hTid-1 offer insights into the underlying mechanisms of disease pathogenesis and suggest hTid-1 as a potential therapeutic target.
CELL COMMUNICATION AND SIGNALING
(2022)
Article
Biochemical Research Methods
Jordane Preto, Isabelle Krimm
Summary: The voltage-dependent anion channel (VDAC) is a critical membrane protein in the mitochondrial outer membrane that regulates ion and ATP transport while playing a key role in apoptosis. The N-terminus of VDAC is an intrinsically disordered region that significantly impacts its gating mechanism, providing new insights into the dynamics of the channel.
PLOS COMPUTATIONAL BIOLOGY
(2021)
Article
Cell Biology
Elizabeth A. Thompson, Katherine Cascino, Alvaro A. Ordonez, Weiqiang Zhou, Ajay Vaghasia, Anne Hamacher-Brady, Nathan R. Brady, Im-Hong Sun, Rulin Wang, Avi Z. Rosenberg, Michael Delannoy, Richard Rothman, Katherine Fenstermacher, Lauren Sauer, Kathyrn Shaw-Saliba, Evan M. Bloch, Andrew D. Redd, Aaron A. R. Tobian, Maureen Horton, Kellie Smith, Andrew Pekosz, Franco R. D'Alessio, Srinivasan Yegnasubramanian, Hongkai Ji, Andrea L. Cox, Jonathan D. Powell
Summary: The study identifies a unique population of T cells expressing increased VDAC1 in severe and recovered COVID-19 patients, associated with mitochondrial dysfunction and apoptosis. Additionally, specific metabolic phenotypes of myeloid-derived suppressor cells in COVID-19 patients can distinguish between severe and mild disease. These findings offer insight into dysfunctional immune response in COVID-19 patients and potential for developing personalized therapeutic approaches.
Review
Biochemistry & Molecular Biology
Mariana Yolotzin Garcia-Bermudez, Rupali Vohra, Kristine Freude, Peter van Wijngaardenan, Keith Martin, Maj Schneider Thomsen, Blanca Irene Aldana, Miriam Kolko
Summary: This review discusses the diagnostic challenges of Alzheimer's disease (AD) and emphasizes the potential of using retinal alterations as early indicators. It highlights the complexity introduced by the similarities shared with other retinal diseases in the search for AD-specific markers. The review provides a comprehensive overview of the current landscape in AD diagnosis and highlights avenues for progress through retinal examination.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Cell Biology
Filomena Broeskamp, Elizabeth S. M. Edrich, Oskar Knittelfelder, Lisa Neuhaus, Thorsten Meyer, Jonas Heyden, Lukas Habernig, Florian Kreppel, Campbell W. Gourlay, Patrick Rockenfeller
Summary: This study investigated the impact of mitochondrial outer membrane protein Por1 on yeast autophagy, showing that POR1 deficiency reduces autophagic capacity and alters organelle and lipid homeostasis. It was found that the reduced autophagy caused by POR1 deficiency could be circumvented by overexpression of Psd1, suggesting a role for Por1 in Psd1-mediated autophagy regulation.
Article
Medicine, Research & Experimental
Jihoon Han, Heejin Park, Chinmoyee Maharana, A-Ryeong Gwon, Jinsu Park, Seung Hyun Baek, Han-Gyu Bae, Yoonsuk Cho, Hark Kyun Kim, Jae Hoon Sul, Jeongmi Lee, Eunae Kim, Junsik Kim, Yongeun Cho, Sunyoung Park, Leon F. Palomera, Thiruma Arumugam, Mark P. Mattson, Dong-Gyu Jo
Summary: The five FAD-linked PS1 mutations have been shown to have deleterious effects on mitochondrial functions in different ways. Each PS1 mutant affected mitochondrial morphology and function differently, with some inducing mitochondrial fragmentation while others increased MAMs formation and oxidative stress. These mutations compromised mitochondrial membrane potential and ATP production, which may contribute to an accelerated age of disease onset in individuals with mutant PS1.
Article
Oncology
Srinivas Pittala, Yakov Krelin, Varda Shoshan-Barmatz
Article
Oncology
Tasleem Arif, Avijit Paul, Yakov Krelin, Anna Shteinfer-Kuzmine, Varda Shoshan-Barmatz
Review
Biochemistry & Molecular Biology
Varda Shoshan-Barmatz, Srinivas Pittala, Dario Mizrachi
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2019)
Article
Biotechnology & Applied Microbiology
Srinivas Pittala, Yakov Krelin, Yael Kuperman, Varda Shoshan-Barmatz
Article
Cell Biology
Tasleem Arif, Oriel Stern, Srinivas Pittala, Vered Chalifa-Caspi, Varda Shoshan-Barmatz
Article
Cell Biology
Srinivas Pittala, Idan Levy, Soumasree De, Swaroop Kumar Pandey, Nataly Melnikov, Tehila Hyman, Varda Shoshan-Barmatz
Article
Oncology
Zohar Amsalem, Tasleem Arif, Anna Shteinfer-Kuzmine, Vered Chalifa-Caspi, Varda Shoshan-Barmatz
Article
Oncology
Erez Zerbib, Tasleem Arif, Anna Shteinfer-Kuzmine, Vered Chalifa-Caspi, Varda Shoshan-Barmatz
Summary: Tumors consist of proliferating cancer cells and their microenvironment, including extracellular matrix, blood vessels, and tissue cells. Understanding molecular interactions between cancer cells and the microenvironment is crucial for developing therapeutic strategies. Depleting VDAC1 in cancer cells leads to metabolic reprogramming, inhibits tumor growth, and disrupts tumor-host interactions, making it a potential therapeutic target for inhibiting cancer progression.
Editorial Material
Oncology
Joao Pessoa, Marta Martins, Sandra Casimiro, Carlos Perez-Plasencia, Varda Shoshan-Barmatz
FRONTIERS IN ONCOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Swaroop Kumar Pandey, Renen Machlof-Cohen, Manikandan Santhanam, Anna Shteinfer-Kuzmine, Varda Shoshan-Barmatz
Summary: This study found that VDAC1 is overexpressed in patients with mesothelioma and its levels increase with disease stage, leading to low survival rates. Silencing VDAC1 expression can inhibit cell proliferation of mesothelioma cancer cells and cause metabolic reprogramming. VDAC1 silencing also has effects on modulating the tumor microenvironment and inflammation, eliminating cancer stem cells, and inducing cell differentiation.
Article
Biochemistry & Molecular Biology
Anna Shteinfer-Kuzmine, Shirel Argueti-Ostrovsky, Marcel F. Leyton-Jaimes, Uttpal Anand, Salah Abu-Hamad, Ran Zalk, Varda Shoshan-Barmatz, Adrian Israelson
Summary: This study suggests that the interaction between VDAC1 and SOD1 is involved in the pathogenesis of ALS. By inhibiting VDAC1 oligomerization, it is possible to reduce cell apoptosis and related processes caused by mutant SOD1, thus improving muscle function in ALS patients.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Biochemistry & Molecular Biology
Uttpal Anand, Anna Shteinfer-Kuzmine, Gal Sela, Manikandan Santhanam, Benjamin Gottschalk, Rajaa Boujemaa-Paterski, Ohad Medalia, Wolfgang F. Graier, Varda Shoshan-Barmatz
Summary: The mitochondrial protein VDAC1 plays a crucial role in regulating various cellular processes, including metabolism, apoptosis, and cell signaling. In this study, a short peptide derived from the N-terminal region of VDAC1 was designed to improve cellular stability and activity. The peptide exhibited multiple effects on cancer cells, such as apoptosis induction, autophagy, senescence, and cell adhesion. Furthermore, the peptide altered the expression of proteins associated with cell metabolism and signaling. These findings highlight the importance of VDAC1 in controlling diverse cellular functions through its interaction with other proteins.
Article
Oncology
Almog Nadir, Anna Shteinfer-Kuzmine, Swaroop Kumar Pandey, Juan Ortas, Daniel Kerekes, Varda Shoshan-Barmatz
Summary: This study identified three different plant extracts that can effectively induce cell death and focused on the most potent extract. The extract kills tumor cells through multiple mechanisms, including impairing cell energy and metabolism, generating reactive oxygen species, increasing intracellular calcium levels, and inducing mitochondria-mediated apoptosis. In a mouse model of glioblastoma, the extract inhibits tumor growth and induces massive tumor cell death, including cancer stem cells, by inhibiting blood supply and modulating the tumor microenvironment. These findings suggest that the plant extract has potential as a cancer therapeutic.
Review
Biochemistry & Molecular Biology
Varda Shoshan-Barmatz, Anna Shteinfer-Kuzmine, Ankit Verma