Nathan A Ungerleider
Overview
Explore the profile of Nathan A Ungerleider including associated specialties, affiliations and a list of published articles.
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Articles
16
Citations
343
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Recent Articles
1.
Murray-Nerger L, Lozano C, Burton E, Liao Y, Ungerleider N, Guo R, et al.
Nat Commun
. 2024 May;
15(1):4156.
PMID: 38755141
Epstein-Barr virus (EBV) uses a biphasic lifecycle of latency and lytic reactivation to infect >95% of adults worldwide. Despite its central role in EBV persistence and oncogenesis, much remains unknown...
2.
Ungerleider N, Roberts C, OGrady T, Nguyen T, Baddoo M, Wang J, et al.
Nucleic Acids Res
. 2024 Mar;
52(9):5016-5032.
PMID: 38471819
Viruses are master remodelers of the host cell environment in support of infection and virus production. For example, viruses typically regulate cell gene expression through modulating canonical cell promoter activity....
3.
Abdulnour-Nakhoul S, Kolls J, Flemington E, Ungerleider N, Nakhoul H, Song K, et al.
Am J Physiol Gastrointest Liver Physiol
. 2024 Jan;
326(4):G438-G459.
PMID: 38193195
The calcium-sensing receptor (CaSR), a G protein-coupled receptor, regulates Ca concentration in plasma by regulating parathyroid hormone secretion. In other tissues, it is reported to play roles in cellular differentiation...
4.
Flemington E, Flemington S, OGrady T, Baddoo M, Nguyen T, Dong Y, et al.
Nucleic Acids Res
. 2023 Mar;
51(7):e42.
PMID: 36864749
As a fundamental aspect of normal cell signaling and disease states, there is great interest in determining alternative splicing (AS) changes in physiologic, pathologic, and pharmacologic settings. High throughput RNA...
5.
OGrady T, Baddoo M, Flemington S, Ishaq E, Ungerleider N, Flemington E
Front Immunol
. 2023 Jan;
13:1060114.
PMID: 36601126
Introduction: B cell activation and differentiation is central to the adaptive immune response. Changes in exon usage can have major impacts on cellular signaling and differentiation but have not been...
6.
Shahbandi A, Chiu F, Ungerleider N, Kvadas R, Mheidly Z, Sun M, et al.
Nat Cancer
. 2022 Dec;
3(12):1513-1533.
PMID: 36482233
Breast cancer cells must avoid intrinsic and extrinsic cell death to relapse following chemotherapy. Entering senescence enables survival from mitotic catastrophe, apoptosis and nutrient deprivation, but mechanisms of immune evasion...
7.
Melnik L, Guha S, Ghimire J, Smither A, Beddingfield B, Hoffmann A, et al.
Cell Rep
. 2022 Jan;
38(1):110172.
PMID: 34986351
During the 2013-2016 West African (WA) Ebola virus (EBOV) outbreak, severe gastrointestinal symptoms were common in patients and associated with poor outcome. Delta peptide is a conserved product of post-translational...
8.
Galati M, Hodel K, Gams M, Sudhaman S, Bridge T, Zahurancik W, et al.
Cancer Res
. 2020 Sep;
80(24):5606-5618.
PMID: 32938641
mutations are a major cause of hypermutant cancers, yet questions remain regarding mechanisms of tumorigenesis, genotype-phenotype correlation, and therapeutic considerations. In this study, we establish mouse models harboring cancer-associated mutations...
9.
Shahbandi A, Rao S, Anderson A, Frey W, Olayiwola J, Ungerleider N, et al.
Cell Death Differ
. 2020 May;
27(11):3097-3116.
PMID: 32457483
TP53 wild-type breast tumors rarely undergo a complete pathological response after chemotherapy treatment. These patients have an extremely poor survival rate and studies show these tumors preferentially undergo senescence instead...
10.
Tonnessen-Murray C, Frey W, Rao S, Shahbandi A, Ungerleider N, Olayiwola J, et al.
J Cell Biol
. 2019 Sep;
218(11):3827-3844.
PMID: 31530580
In chemotherapy-treated breast cancer, wild-type p53 preferentially induces senescence over apoptosis, resulting in a persisting cell population constituting residual disease that drives relapse and poor patient survival via the senescence-associated...