David W Morgens
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Explore the profile of David W Morgens including associated specialties, affiliations and a list of published articles.
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41
Citations
2695
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Recent Articles
11.
Gruninger P, Uhl F, Herzog H, Gentile G, Andrade-Martinez M, Schmidt T, et al.
Cancer Gene Ther
. 2022 Jul;
29(11):1751-1760.
PMID: 35794338
B-cell precursor acute lymphoblastic leukemias (B-ALL) are characterized by the activation of signaling pathways, which are involved in survival and proliferation of leukemia cells. Using an unbiased shRNA library screen...
12.
Morgens D, Nandakumar D, Didychuk A, Yang K, Glaunsinger B
PLoS Pathog
. 2022 Jan;
18(1):e1010236.
PMID: 35041709
While traditional methods for studying large DNA viruses allow the creation of individual mutants, CRISPR/Cas9 can be used to rapidly create thousands of mutant dsDNA viruses in parallel, enabling the...
13.
Bieging-Rolett K, Kaiser A, Morgens D, Boutelle A, Seoane J, Van Nostrand E, et al.
Mol Cell
. 2020 Nov;
80(3):452-469.e9.
PMID: 33157015
Although TP53 is the most commonly mutated gene in human cancers, the p53-dependent transcriptional programs mediating tumor suppression remain incompletely understood. Here, to uncover critical components downstream of p53 in...
14.
Marschallinger J, Iram T, Zardeneta M, Lee S, Lehallier B, Haney M, et al.
Nat Neurosci
. 2020 Jul;
23(10):1308.
PMID: 32719564
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
15.
Dubreuil M, Morgens D, Okumoto K, Honsho M, Contrepois K, Lee-McMullen B, et al.
Cell Rep
. 2020 Feb;
30(5):1417-1433.e7.
PMID: 32023459
Reactive oxygen species (ROS) play critical roles in metabolism and disease, yet a comprehensive analysis of the cellular response to oxidative stress is lacking. To systematically identify regulators of oxidative...
16.
Marschallinger J, Iram T, Zardeneta M, Lee S, Lehallier B, Haney M, et al.
Nat Neurosci
. 2020 Feb;
23(2):294.
PMID: 32005940
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
17.
Marschallinger J, Iram T, Zardeneta M, Lee S, Lehallier B, Haney M, et al.
Nat Neurosci
. 2020 Jan;
23(2):194-208.
PMID: 31959936
Microglia become progressively activated and seemingly dysfunctional with age, and genetic studies have linked these cells to the pathogenesis of a growing number of neurodegenerative diseases. Here we report a...
18.
Chai N, Haney M, Couthouis J, Morgens D, Benjamin A, Wu K, et al.
Brain Res
. 2019 Dec;
1728:146601.
PMID: 31843624
Mutations in the C9ORF72 gene are the most common cause of amyotrophic lateral sclerosis (ALS). Both toxic gain of function and loss of function pathogenic mechanisms have been proposed. Accruing...
19.
Morgens D, Chan C, Kane A, Weir N, Li A, Dubreuil M, et al.
Elife
. 2019 Nov;
8.
PMID: 31674906
The small molecule Retro-2 prevents ricin toxicity through a poorly-defined mechanism of action (MOA), which involves halting retrograde vesicle transport to the endoplasmic reticulum (ER). CRISPRi genetic interaction analysis revealed...
20.
Cheng W, Wang S, Zhang Z, Morgens D, Hayes L, Lee S, et al.
Neuron
. 2019 Oct;
104(5):885-898.e8.
PMID: 31587919
Hexanucleotide GGGGCC repeat expansion in C9ORF72 is the most prevalent genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). One pathogenic mechanism is the aberrant accumulation of dipeptide...