Author

T. L. Pulliam

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

Biology Disciplines

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Cancer Biology· 4

Signature Assays, Organisms & Methods

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Research Focus:cancer & tumor microenvironment· 3 Approach:experimental assay· 3 Research Focus:drug response / drug discovery· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:differential expression· 1 Approach:genetic perturbation / CRISPR· 1 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

D. E. Frigo· 4 shared D. Awad· 3 shared J. J. Han· 3 shared M. M. Ittmann· 3 shared M. M. Murray· 3 shared C. Lin· 2 shared J. J. Ackroyd· 2 shared J. S. Oakhill· 2 shared

Activity by Year

2020-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 40 mutual co-author links

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4 shared papersCancer Biology

D. E. Frigo

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Author profile →

4 papers

Recent·Most cited

SGC-CAMKK2-1: A chemical probe for CAMKK2

C. I. Wells, Y. Liang, T. L. Pulliam, C. Lin, D. Awad, B. Eduful, S. O Byrne, M. A. Hossain, C. Catta-Preta, P. Zonzini Ramos, O. Gileadi, C. Gileadi, R. M. Counago, B. Stork, C. G. Langendorf, , D. H. Drewry

This paper introduces SGC-CAMKK2-1, a selective chemical probe for CAMKK2, demonstrating its potential as a tool to study the therapeutic benefits of CAMKK2 inhibition.

Cells · Jan 11, 2023Peer-reviewedCancer Biology

Adipose triglyceride lipase is regulated by CAMKK2-AMPK signaling and drives advanced prostate cancer

D. Awad, T. L. Pulliam, M. L. Spradlin, P. H.-A. Cao, E. Subramani, T. V. Tellman, C. F. Ribeiro, H. Pakula, J. J. Ackroyd, M. M. Murray, J. J. Han, B. Piyarathna, J. M. Drake, M. M. Ittmann, C. Coarfa, , D. E. Frigo

This study identifies ATGL as a CAMKK2-AMPK target that promotes CRPC progression by enhancing lipase activity and metabolic plasticity, suggesting it as a therapeutic target.

bioRxiv · Nov 2, 2022 · PreprintCancer Biology

Systemic ablation of Camkk2 impairs metastatic colonization and improves insulin sensitivity in TRAMP mice: Evidence for cancer cell-extrinsic CAMKK2 functions in prostate cancer

T. L. Pulliam, D. Awad, J. J. Han, M. M. Murray, J. J. Ackroyd, P. Goli, J. S. Oakhill, J. W. Scott, M. M. Ittmann, D. E. Frigo

This study shows that deleting Camkk2 in TRAMP mice reduces metastasis and improves insulin sensitivity, suggesting CAMKK2 has non-autonomous roles in prostate cancer progression.

bioRxiv · Mar 28, 2022Cancer Biology

Inhibition of CAMKK2 impairs autophagy and castration-resistant prostate cancer via suppression of AMPK-ULK1 signaling

C. Lin, A. M. Blessing, T. L. Pulliam, Y. Shi, S. R. Wilkenfeld, J. J. Han, M. M. Murray, A. H. Pham, K. Duong, S. N. Brun, R. J. Shaw, M. M. Ittmann, D. E. Frigo

This study shows that inhibiting CAMKK2 blocks autophagy and slows castration-resistant prostate cancer by disrupting AMPK-ULK1 signaling.

bioRxiv · Jun 2, 2020Cancer Biology