His main research concerns Cell biology, Neuroscience, Neurodegeneration, Mutant and Programmed cell death. His Cell biology research includes themes of Neurotrophic factors and Biochemistry, Gene. His Neuroscience research incorporates elements of Glutamate receptor and CREB.
Steven Finkbeiner has researched Neurodegeneration in several fields, including DNAJA3 and Amyotrophic lateral sclerosis. As a member of one scientific family, Steven Finkbeiner mostly works in the field of Mutant, focusing on Mutation and, on occasion, Stem cell and Autophagy. His work deals with themes such as Autophagosome, MAP1LC3B, Sequestosome 1, Computational biology and Physiology, which intersect with Programmed cell death.
His primary areas of study are Neuroscience, Cell biology, Neurodegeneration, Huntingtin and Disease. The various areas that Steven Finkbeiner examines in his Neuroscience study include Synaptic plasticity, Amyotrophic lateral sclerosis, Cell type and Induced pluripotent stem cell. His studies deal with areas such as Autophagy, Genetics, Neurotrophic factors, Mutant and Inclusion bodies as well as Cell biology.
His Autophagy research includes elements of Lysosome and Neuroprotection. His Neurodegeneration research is multidisciplinary, relying on both Frontotemporal dementia, Proteostasis, Biochemistry, Molecular biology and Programmed cell death. Steven Finkbeiner specializes in Huntingtin, namely Huntingtin Protein.
Steven Finkbeiner focuses on Neuroscience, Cell biology, Neurodegeneration, Autophagy and Disease. His studies in Neuroscience integrate themes in fields like Synaptic plasticity, Huntington's disease and Homeostatic plasticity. His research in Cell biology intersects with topics in Stress granule, Huntingtin, Neuron and Phenotype.
His study in Neurodegeneration is interdisciplinary in nature, drawing from both Pathogenesis, Parkinson's disease, Alpha-synuclein, Single-cell analysis and Proteostasis. His Autophagy study combines topics in areas such as Loss function, Lysosome, Frontotemporal dementia, Neuronal ceroid lipofuscinosis and Haploinsufficiency. His Programmed cell death research is multidisciplinary, incorporating elements of Chaperone-mediated autophagy, Autolysosome and Knowledge base.
Steven Finkbeiner mostly deals with Computational biology, Artificial intelligence, Deep learning, Pattern recognition and Systems biology. The study incorporates disciplines such as Gene Discovery, Genome, Intellectual disability, Autolysosome and Als gene in addition to Computational biology. His Artificial intelligence study integrates concerns from other disciplines, such as In silico, Cell state and Antibody labeling.
His study in Deep learning is interdisciplinary in nature, drawing from both Artificial neural network, Pixel and Hoechst stain. Steven Finkbeiner integrates Pattern recognition with Focus in his research. The concepts of his Systems biology study are interwoven with issues in Infectious disease, Genomic data, Interactome and Neurodevelopmental disorder.
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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)
Daniel J. Klionsky;Amal Kamal Abdel-Aziz;Sara Abdelfatah;Mahmoud Abdellatif.
Autophagy (2021)
Guidelines for the use and interpretation of assays for monitoring autophagy
Daniel J. Klionsky;Fabio C. Abdalla;Hagai Abeliovich;Robert T. Abraham.
Autophagy (2012)
Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)
Daniel J. Klionsky;Kotb Abdelmohsen;Akihisa Abe;Joynal Abedin.
Autophagy (2016)
Glutamate induces calcium waves in cultured astrocytes: long-range glial signaling
Ann H. Cornell-Bell;Steven M. Finkbeiner;Mark S. Cooper;Stephen J. Smith.
Science (1990)
Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death
Montserrat Arrasate;Siddhartha Mitra;Erik S. Schweitzer;Mark R. Segal.
Nature (2004)
Huntingtin Acts in the Nucleus to Induce Apoptosis but Death Does Not Correlate with the Formation of Intranuclear Inclusions
Frédéric Saudou;Frédéric Saudou;Steven Finkbeiner;Steven Finkbeiner;Didier Devys;Michael E Greenberg;Michael E Greenberg.
Cell (1998)
Ca2+ Influx Regulates BDNF Transcription by a CREB Family Transcription Factor-Dependent Mechanism
Xu Tao;Steven Finkbeiner;Donald B. Arnold;Adam J. Shaywitz.
Neuron (1998)
Aberrant Excitatory Neuronal Activity and Compensatory Remodeling of Inhibitory Hippocampal Circuits in Mouse Models of Alzheimer's Disease
Jorge J. Palop;Jeannie Chin;Erik D. Roberson;Jun Wang.
Neuron (2007)
CREB: A Major Mediator of Neuronal Neurotrophin Responses
Steven Finkbeiner;Sohail F Tavazoie;Anna Maloratsky;Kori M Jacobs.
Neuron (1997)
Identification of novel risk loci, causal insights, and heritable risk for Parkinson's disease: a meta-analysis of genome-wide association studies
Mike A Nalls;Cornelis Blauwendraat;Costanza L Vallerga;Karl Heilbron.
Lancet Neurology (2019)
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