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Boaz Barak

Showing results (31-40 of 51) with videos related to

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Cell Reports|July 24, 2025
Cell-of-origin-specific behavioral deficits in oligodendrocyte-derived glioblastomaDivsha Sher, Ignacio Mastandrea, Alina Brosque, et al.
Glia|March 7, 2024
Neuronal deletion of Gtf2i results in developmental microglial alterations in a mouse model related to Williams syndromeEla Bar, Inbar Fischer, May Rokach, et al.
Molecular Psychiatry|July 11, 2018
Shank3 mutation in a mouse model of autism leads to changes in the S-nitroso-proteome and affects key proteins involved in vesicle release and synaptic functionHaitham Amal, Boaz Barak, Vadiraja Bhat, et al.
ACS Applied Materials & Interfaces|June 26, 2012
Highly ordered large-scale neuronal networks of individual cells - toward single cell to 3D nanowire intracellular interfacesMoria Kwiat, Roey Elnathan, Alexander Pevzner, et al.
Frontiers in Neuroanatomy|December 31, 2010
Tomosyn expression pattern in the mouse hippocampus suggests both presynaptic and postsynaptic functionsBoaz Barak, Antionette Williams, Noa Bielopolski, et al.
Proceedings of the National Academy of Sciences of the United States of America|August 18, 2010
Toll-like receptor 3 inhibits memory retention and constrains adult hippocampal neurogenesisEitan Okun, Kathleen Griffioen, Boaz Barak, et al.
Molecular Psychiatry|May 10, 2022
SH3- and actin-binding domains connect ADNP and SHANK3, revealing a fundamental shared mechanism underlying autismYanina Ivashko-Pachima, Maram Ganaiem, Inbar Ben-Horin-Hazak, et al.
Nature Neuroscience|April 24, 2019
Neuronal deletion of Gtf2i, associated with Williams syndrome, causes behavioral and myelin alterations rescuable by a remyelinating drugBoaz Barak, Zicong Zhang, Yuanyuan Liu, et al.
Nature Neuroscience|June 8, 2019
Publisher Correction: Neuronal deletion of Gtf2i, associated with Williams syndrome, causes behavioral and myelin alterations rescuable by a remyelinating drugBoaz Barak, Zicong Zhang, Yuanyuan Liu, et al.
Communications Biology|December 14, 2023
Neuronal Gtf2i deletion alters mitochondrial and autophagic propertiesAriel Nir Sade, Gilad Levy, Sari Schokoroy Trangle, et al.
Pageof 6

Showing results (31-40 of 51) with videos related to

Sort By:
Pageof 6
Cell Reports|July 24, 2025
Cell-of-origin-specific behavioral deficits in oligodendrocyte-derived glioblastomaDivsha Sher, Ignacio Mastandrea, Alina Brosque, et al.
Glia|March 7, 2024
Neuronal deletion of Gtf2i results in developmental microglial alterations in a mouse model related to Williams syndromeEla Bar, Inbar Fischer, May Rokach, et al.
Molecular Psychiatry|July 11, 2018
Shank3 mutation in a mouse model of autism leads to changes in the S-nitroso-proteome and affects key proteins involved in vesicle release and synaptic functionHaitham Amal, Boaz Barak, Vadiraja Bhat, et al.
ACS Applied Materials & Interfaces|June 26, 2012
Highly ordered large-scale neuronal networks of individual cells - toward single cell to 3D nanowire intracellular interfacesMoria Kwiat, Roey Elnathan, Alexander Pevzner, et al.
Frontiers in Neuroanatomy|December 31, 2010
Tomosyn expression pattern in the mouse hippocampus suggests both presynaptic and postsynaptic functionsBoaz Barak, Antionette Williams, Noa Bielopolski, et al.
Proceedings of the National Academy of Sciences of the United States of America|August 18, 2010
Toll-like receptor 3 inhibits memory retention and constrains adult hippocampal neurogenesisEitan Okun, Kathleen Griffioen, Boaz Barak, et al.
Molecular Psychiatry|May 10, 2022
SH3- and actin-binding domains connect ADNP and SHANK3, revealing a fundamental shared mechanism underlying autismYanina Ivashko-Pachima, Maram Ganaiem, Inbar Ben-Horin-Hazak, et al.
Nature Neuroscience|April 24, 2019
Neuronal deletion of Gtf2i, associated with Williams syndrome, causes behavioral and myelin alterations rescuable by a remyelinating drugBoaz Barak, Zicong Zhang, Yuanyuan Liu, et al.
Nature Neuroscience|June 8, 2019
Publisher Correction: Neuronal deletion of Gtf2i, associated with Williams syndrome, causes behavioral and myelin alterations rescuable by a remyelinating drugBoaz Barak, Zicong Zhang, Yuanyuan Liu, et al.
Communications Biology|December 14, 2023
Neuronal Gtf2i deletion alters mitochondrial and autophagic propertiesAriel Nir Sade, Gilad Levy, Sari Schokoroy Trangle, et al.
Pageof 6