User profiles for J. K. Ichida

Justin Ichida

University of Southern California
Verified email at usc.edu
Cited by 6716

[PDF][PDF] A small-molecule inhibitor of Tgf-β signaling replaces Sox2 in reprogramming by inducing Nanog

JK Ichida, J Blanchard, K Lam, EY Son, JE Chung… - Cell stem cell, 2009 - cell.com
The combined activity of three transcription factors can reprogram adult cells into induced
pluripotent stem cells (iPSCs). However, the transgenic methods used for delivering …

[PDF][PDF] Conversion of mouse and human fibroblasts into functional spinal motor neurons

EY Son, JK Ichida, BJ Wainger, JS Toma, VF Rafuse… - Cell stem cell, 2011 - cell.com
The mammalian nervous system comprises many distinct neuronal subtypes, each with its
own phenotype and differential sensitivity to degenerative disease. Although specific …

[PDF][PDF] Antisense proline-arginine RAN dipeptides linked to C9ORF72-ALS/FTD form toxic nuclear aggregates that initiate in vitro and in vivo neuronal death

…, J Monaghan, UB Pandey, P Pasinelli, JK Ichida… - Neuron, 2014 - cell.com
Expanded GGGGCC (G4C2) nucleotide repeats within the C9ORF72 gene are the most
common genetic mutation associated with both amyotrophic lateral sclerosis (ALS) and …

Haploinsufficiency leads to neurodegeneration in C9ORF72 ALS/FTD human induced motor neurons

…, RJ Pasterkamp, D Trotti, BV Zlokovic, JK Ichida - Nature medicine, 2018 - nature.com
An intronic GGGGCC repeat expansion in C9ORF72 is the most common cause of
amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), but the pathogenic …

Central role for PICALM in amyloid-β blood-brain barrier transcytosis and clearance

…, M Maeda, T Maeda, T Sugawara, JK Ichida… - Nature …, 2015 - nature.com
PICALM is a highly validated genetic risk factor for Alzheimer's disease (AD). We found that
reduced expression of PICALM in AD and murine brain endothelium correlated with amyloid-…

Probing disorders of the nervous system using reprogramming approaches

JK Ichida, E Kiskinis - The EMBO journal, 2015 - embopress.org
The groundbreaking technologies of induced pluripotency and lineage conversion have
generated a genuine opportunity to address fundamental aspects of the diseases that affect the …

CRISPR–Cas9 screens in human cells and primary neurons identify modifiers of C9ORF72 dipeptide-repeat-protein toxicity

…, Y Shi, NT Hertz, M Tessier-Lavigne, JK Ichida… - Nature …, 2018 - nature.com
Hexanucleotide-repeat expansions in the C9ORF72 gene are the most common cause of
amyotrophic lateral sclerosis and frontotemporal dementia (c9ALS/FTD). The nucleotide-…

Modeling pain in vitro using nociceptor neurons reprogrammed from fibroblasts

…, C Mellin, S Lee, WA Saber, AJ Wang, JK Ichida… - Nature …, 2015 - nature.com
Reprogramming somatic cells from one cell fate to another can generate specific neurons
suitable for disease modeling. To maximize the utility of patient-derived neurons, they must …

[PDF][PDF] ELAVL4, splicing, and glutamatergic dysfunction precede neuron loss in MAPT mutation cerebral organoids

…, K Lane, JF Crary, SJ Haggarty, CM Karch, JK Ichida… - Cell, 2021 - cell.com
Frontotemporal dementia (FTD) because of MAPT mutation causes pathological accumulation
of tau and glutamatergic cortical neuronal death by unknown mechanisms. We used …

[PDF][PDF] p53 is a central regulator driving neurodegeneration caused by C9orf72 poly (PR)

…, M Tessier-Lavigne, LD Attardi, TE Lloyd, JK Ichida… - Cell, 2021 - cell.com
The most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal
dementia (FTD) is a GGGGCC repeat expansion in the C9orf72 gene. We developed a …