Author

N. K. Tangudu

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Cancer Biology· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Organism:human· 3 Approach:genetic perturbation / CRISPR· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:drug response / drug discovery· 1 Approach:experimental assay· 1

Frequent Co-Authors

A. Amalric· 3 shared A. R. Cole· 3 shared A. Uboveja· 3 shared K. M. Aird· 3 shared N. W. Snyder· 3 shared R. Buj· 3 shared B. Yang· 2 shared H. Wang· 2 shared

Activity by Year

2023-2023 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

3 shared papersCancer Biology

A. Amalric

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

The chemotherapy-induced senescence-associated secretome promotes cell detachment and metastatic dissemination through metabolic reprogramming

A. R. Cole, R. Buj, A. Uboveja, E. Levasseur, H. Wang, K. M. Kedziora, A. Chatoff, A. Andress Huacachino, M. M. Marcinkiewicz, A. Amalric, B. Yang, N. K. Tangudu, J. Danielson, A. Taher Elhaw, S. White, , K. M. Aird

This study shows that chemotherapy-induced senescence-associated secretome promotes metastasis in ovarian cancer by reprogramming metabolism and increasing cell detachment.

bioRxiv · Dec 2, 2023Cancer Biology

ATR promotes mTORC1 activity via de novo cholesterol synthesis

N. K. Tangudu, A. N. Grumet, R. Fang, R. Buj, A. R. Cole, A. Uboveja, A. Amalric, B. Yang, Z. Huang, C. Happe, M. Sun, S. L. Gelhaus, M. L. MacDonald, N. Hempel, N. W. Snyder, , K. M. Aird

This study shows ATR enhances mTORC1 activity through cholesterol synthesis via LSS, independent of CHK1 and TSC, and this effect is amplified in p16-deficient cells.

bioRxiv · Oct 27, 2023Cell Biology

De novo purine metabolism is a metabolic vulnerability of cancers with low p16 expression

N. K. Tangudu, R. Buj, H. Wang, J. Wang, A. R. Cole, A. Uboveja, R. Fang, A. Amalric, P. Sajjakulnukit, M. A. Lyons, K. Cooper, N. W. Hempel, N. W. Snyder, C. A. Lyssiotis, U. R. Chandran, K. M. Aird

This study identifies de novo purine metabolism as a vulnerability in cancers with low p16 expression, showing sensitivity to anti-folate drugs like methotrexate.

bioRxiv · Jul 15, 2023Cancer Biology