Gregory Caleb Howard's research while affiliated with Vanderbilt University and other places

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Publications (2)

Ribosome subunit attrition and activation of the p53–MDM4 axis dominate the response of MLL-rearranged cancer cells to WDR5 WIN site inhibition
Article
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  • Apr 2024
The chromatin-associated protein WD Repeat Domain 5 (WDR5) is a promising target for cancer drug discovery, with most efforts blocking an arginine-binding cavity on the protein called the ‘WIN’ site that tethers WDR5 to chromatin. WIN site inhibitors (WINi) are active against multiple cancer cell types in vitro, the most notable of which are those...
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MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with host cell factor–1
Article
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  • Jan 2021
The oncoprotein transcription factor MYC is a major driver of malignancy and a highly validated but challenging target for the development of anticancer therapies. Novel strategies to inhibit MYC may come from understanding the co-factors it uses to drive pro-tumorigenic gene expression programs, providing their role in MYC activity is understood....
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... Notably, TF-bound targets of MYC, MAX, and HCF1 overlapped highly with each other, with these bound targets also overlapping genes with lower expression with MYC or MAX knockdown. Of note, MAX is essential for MYC's oncogenic function in its dimerization with MYC [36,37], and MYC is known to directly interact with a recruits HCFC1 [36], where the MYC-HCFC1 interaction in particular can regulate mitochondrial gene expression programs among others [36,38,39]. The nonessential signature genes were also significantly enriched for targets of TFs, including MYC, MAX, and HCFC1, though these three TFs involved a relatively lower fraction of genes for the nonessential versus the essential signature ( Fig. 5c and Data File S2). ...
Reference: An essential gene signature of breast cancer metastasis reveals targetable pathways
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