A5071245379- RNA Research and Splicing
- Ubiquitin and proteasome pathways
- CRISPR and Genetic Engineering
- Genomics and Chromatin Dynamics
- Hereditary Neurological Disorders
- Amyotrophic Lateral Sclerosis Research
- Axon Guidance and Neuronal Signaling
- RNA and protein synthesis mechanisms
- Plant Gene Expression Analysis
- Protein Kinase Regulation and GTPase Signaling
- Protein Tyrosine Phosphatases
- Signaling Pathways in Disease
- Plant-Microbe Interactions and Immunity
- CAR-T cell therapy research
- RNA regulation and disease
- Histone Deacetylase Inhibitors Research
- Plant Molecular Biology Research
University of Wisconsin–Madison
2020-2024
California University of Pennsylvania
2024
State Key Laboratory of Plant Genomics
2016
Institute of Genetics and Developmental Biology
2016
Chinese Academy of Sciences
2016
Center for Excellence in Molecular Plant Sciences
2016
Emerging evidences exhibit that mitogen-activated protein kinase (MAPK/MPK) signaling pathways are connected with many aspects of plant development. The complexity MAPK cascades raises challenges not only to identify the module in planta but also define specific role an individual module. So far, our knowledge has been largely restricted a small subset cascades. Our previous study characterized Arabidopsis bushy and dwarf1 (bud1) mutant, which MAP Kinase 7 (MKK7) was constitutively...
Mutations in the ubiquitin (Ub) chaperone Ubiquilin 2 (UBQLN2 ) cause X-linked forms of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) through unknown mechanisms. Here, we show that aggregation-prone, ALS-associated mutants UBQLN2 ALS trigger heat stress-dependent neurodegeneration Drosophila . A genetic modifier screen implicated endolysosomal axon guidance genes, including netrin receptor, Unc-5, as key modulators toxicity. Reduced gene dosage Unc-5 or its coreceptor...
Fused in sarcoma (FUS) encodes an RNA-binding protein with diverse roles transcriptional activation and RNA splicing. While oncogenic fusions of FUS transcription factor DNA-binding domains are associated soft tissue sarcomas, dominant mutations can cause amyotrophic lateral sclerosis. has also been implicated genome maintenance. However, the underlying mechanisms its actions stability unknown. Here, we applied gene editing, functional reconstitution, integrated proteomics transcriptomics to...
The cAMP response element-binding protein (CREB) is an important regulator of cell growth, metabolism, and synaptic plasticity. CREB activated through phosphorylation evolutionarily conserved Ser residue (S133) within its intrinsically disordered kinase-inducible domain (KID). Phosphorylation S133 in to cAMP, Ca2+, other stimuli triggers association the KID with KID-interacting (KIX) CREB-binding (CBP), a histone acetyl transferase (HAT) that promotes transcriptional activation. Here we...
This protocol was designed for the workflow of Multiome assay on 16 PBMC samples using 10X Next GEM Single Cell ATAC + Gene Expression Kit. We adapted Jimmy Ye Lab's pooling and demultiplexing strategy, overloading cells in each well. For step this protocol, you may need genotyping information your samples.
ABSTRACT RIF1 (RAP1 interacting factor) fulfills diverse roles in DNA double-strand break repair, replication, and nuclear organization. is expressed as two splice variants, RIF1-Long (RIF1-L) RIF1-Short (RIF1-S), from the alternative splicing (AS) of Exon 32 (Ex32) which encodes a 26 aa Ser/Lys-rich cassette peptide C-terminal domain (CTD). Here we demonstrate that Ex32 inclusion was repressed by damage oncogenesis but peaked at G 2 /M phase cell cycle. splice-in catalyzed positive...
Abstract Fused in sarcoma (FUS ) encodes a low complexity RNA-binding protein with diverse roles transcriptional activation and RNA processing. While oncogenic fusions of FUS transcription factor DNA-binding domains are associated soft tissue sarcomas, dominant mutations cause amyotrophic lateral sclerosis (ALS) frontotemporal dementia (FTD). has also been implicated DNA double-strand break repair (DSBR) genome maintenance. However, the underlying mechanisms unknown. Here we employed...
Abstract Mutations in the ubiquitin (Ub) chaperone Ubiquilin 2 (UBQLN2) cause X-linked forms of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) through unknown mechanisms. Here we show that aggregation-prone, ALS-associated mutants UBQLN2 (UBQLN2 ALS ) trigger heat stress-dependent neurodegeneration Drosophila. A genetic modifier screen implicated endolysosomal axon guidance genes, including netrin receptor, Unc-5, as key modulators toxicity. Reduced gene dosage Unc-5...