Publications by authors named "M N Orman"

Transcription factors (TFs) are indispensable for maintaining cell identity through regulating cell-specific gene expression. Distinct cell identities derived from a common progenitor are frequently perpetuated by shared TFs, yet the mechanisms that enable these TFs to regulate cell-specific targets are poorly characterized. We report that the TF NKX2.

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Cisplatin-based chemotherapy is used across many common tumor types, but resistance reduces the likelihood of long-term survival. We previously found the puromycin-sensitive aminopeptidase, NPEPPS, as a druggable driver of cisplatin resistance in vitro and in vivo and in patient-derived organoids. Here, we present a general mechanism where NPEPPS interacts with the volume-regulated anion channels (VRACs) to control cisplatin import into cells and thus regulate cisplatin response across a range of cancer types.

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Mutagenic processes drive evolutionary progress, with ultraviolet (UV) radiation significantly affecting evolution. Despite extensive research on SOS response-mediated mutagenesis, UV-induced repair mechanisms remain complex, and their effects on cell survival and mutagenesis are not fully understood. We previously observed a near-perfect correlation between RecA-mediated SOS response and mutation levels in following UV treatment.

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Background: The interactions between bacterial pathogens and host cells are characterized by a multitude of complexities, leading to a wide range of heterogeneous outcomes. Despite extensive research, we still have a limited understanding of how bacterial motility in complex environments impacts their ability to tolerate antibiotics and adhere to mammalian cell surfaces. The challenge lies in unraveling the complexity of these interactions and developing quantitative microscopy approaches to predict the behavior of bacterial populations.

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Article Synopsis
  • Pathogenic mutations in the BRCA1 and BRCA2 genes are linked to several types of hereditary cancer, but inactivating both copies (bBRCA1/2) can be lethal in embryos and reduce cell growth.
  • Researchers identified specific genetic changes commonly found in bBRCA1/2 tumors that could boost cell proliferation and studied them through various analytical methods, including examining mutation patterns in databases.
  • In their results, they discovered that bBRCA1/2 tumors often showed large genomic deletions, identified genes that influenced cell growth, and validated some candidate genes (like RIC8A) as crucial for tumor viability despite the loss of BRCA1 and BRCA2.
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