Bikash Choudhary

Sigmund Freud St. 27
Bonn, NW 53127, Germany

Last Updated: 09/26/2026

Save publications for later
Sign Up
Not sure about your diagnosis?
Check Your Symptoms
Found 8 publications

Regulated microexon alternative splicing in single neurons tunes synaptic function.

Regulated microexon alternative splicing in single neurons tunes synaptic function.

Journal: EMBO reports
Published: January 17, 2025

Conserved role for spliceosomal component PRPF40A in microexon splicing.

Conserved role for spliceosomal component PRPF40A in microexon splicing.

Journal: bioRxiv : the preprint server for biology
Published: October 10, 2024

Conserved role for spliceosomal component PRPF40A in microexon splicing.

Conserved role for spliceosomal component PRPF40A in microexon splicing.

Journal: RNA (New York, N.Y.)
Published: June 18, 2024

Spliceosomal component PRP-40 is a central regulator of microexon splicing.

Spliceosomal component PRP-40 is a central regulator of microexon splicing.

Journal: Cell reports
Published: January 26, 2021

Suppressing Tau Aggregation and Toxicity by an Anti-Aggregant Tau Fragment.

Suppressing Tau Aggregation and Toxicity by an Anti-Aggregant Tau Fragment.

Journal: Molecular neurobiology
Published: June 14, 2018

Glutamatergic nervous system degeneration in a C. elegans TauA152T tauopathy model involves pathways of excitotoxicity and Ca2+ dysregulation.

Glutamatergic nervous system degeneration in a C. elegans TauA152T tauopathy model involves pathways of excitotoxicity and Ca2+ dysregulation.

Journal: Neurobiology of disease
Published: April 20, 2018

UNC-16/JIP3 regulates early events in synaptic vesicle protein trafficking via LRK-1/LRRK2 and AP complexes.

UNC-16/JIP3 regulates early events in synaptic vesicle protein trafficking via LRK-1/LRRK2 and AP complexes.

Journal: PLoS genetics
Published: April 08, 2017

Tau mutant A152T, a risk factor for FTD/PSP, induces neuronal dysfunction and reduced lifespan independently of aggregation in a C. elegans Tauopathy model.

Tau mutant A152T, a risk factor for FTD/PSP, induces neuronal dysfunction and reduced lifespan independently of aggregation in a C. elegans Tauopathy model.

Journal: Molecular neurodegeneration
Published: December 18, 2015
Showing 1-8 of 8

Last Updated: 09/26/2026