Shanni N. Silberberg

ORCID: 0000-0002-7979-9665
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About
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Research Areas
  • Neurogenesis and neuroplasticity mechanisms
  • Single-cell and spatial transcriptomics
  • Genomics and Chromatin Dynamics
  • Neuroscience and Neuropharmacology Research
  • RNA Research and Splicing
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Genetics and Neurodevelopmental Disorders
  • Congenital heart defects research
  • Pluripotent Stem Cells Research
  • Medical Image Segmentation Techniques
  • Developmental Biology and Gene Regulation
  • Genomic variations and chromosomal abnormalities
  • AI in cancer detection

University of California, San Francisco
2013-2022

DLX transcription factors (TFs) are master regulators of the developing vertebrate brain, driving forebrain GABAergic neuronal differentiation. Ablation Dlx1&2 alters expression genes that critical for development. We integrated epigenomic and transcriptomic analyses, complemented with in situ hybridization (ISH), vivo vitro studies regulatory element (RE) function. This revealed DLX-organized gene network at genomic, cellular, spatial levels mouse embryonic basal ganglia. TFs perform dual...

10.1016/j.celrep.2019.07.022 article EN cc-by-nc-nd Cell Reports 2019-08-01

Distinct cortical interneuron (CIN) subtypes have unique circuit functions; dysfunction in specific is implicated neuropsychiatric disorders. Somatostatin- and parvalbumin-expressing (SST+ PV+) interneurons are the two major generated by medial ganglionic eminence (MGE) progenitors. Spatial temporal mechanisms governing their cell-fate specification differential integration into layers largely unknown. We provide evidence that Coup-TF1 Coup-TF2 (Nr2f1 Nr2f2) transcription factor expression...

10.1242/dev.150664 article EN Development 2017-07-11

Enhancers integrate transcription factor signaling pathways that drive cell fate specification in the developing brain. We paired enhancer labeling and single-cell RNA-sequencing (scRNA-seq) to delineate distinguish of neuronal lineages mouse medial, lateral, caudal ganglionic eminences (MGE, LGE, CGE) at embryonic day (E)11.5. show scRNA-seq clustering using factors improves resolution regional developmental populations, activities identify specific overlapping GE-derived populations....

10.1073/pnas.2108760119 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2022-04-04

The medial ganglionic eminence (MGE) is an embryonic forebrain structure that generates the majority of cortical interneurons. MGE transplantation into specific regions postnatal central nervous system modifies circuit function and improves deficits in mouse models epilepsy, Parkinson's disease, pain, phencyclidine-induced cognitive deficits. Herein, we describe approaches to generate MGE-like progenitor cells from stem (ES) cells. Using a modified embryoid body method, provided gene...

10.1371/journal.pone.0061956 article EN cc-by PLoS ONE 2013-05-01

Abstract Enhancers integrate transcription factor signaling pathways that drive cell fate specification in the developing brain. We used single RNA-sequencing (scRNA-seq) to capture enhancer activity at resolution and delineate of cells labeled by enhancers mouse medial, lateral, caudal ganglionic eminences (MGE, LGE, CGE) embryonic day (E)11.5. combine enhancer-based reporter labeling with single-cell transcriptional readout characterize define populations vivo. Seven had diverse activities...

10.1101/2021.01.11.426285 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2021-01-12

DLX transcription factors (TFs) are master regulators of the developing vertebrate brain, driving forebrain GABAergic neuronal differentiation. Ablation Dlx1&2 alters expression genes that critical for development. We integrated epigenomic and transcriptomic analyses, complemented with in situ hybridization (ISH), vivo vitro studies regulatory element (RE) function. This elucidated DLX-organized gene network at genomic, cellular, spatial level mouse embryonic basal ganglia. TFs perform dual...

10.2139/ssrn.3372973 article EN SSRN Electronic Journal 2019-01-01
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