Joshua Rose

ORCID: 0000-0003-2490-7080
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About
Contact & Profiles
Research Areas
  • Epigenetics and DNA Methylation
  • Chronic Obstructive Pulmonary Disease (COPD) Research
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Pulmonary Hypertension Research and Treatments
  • Cancer, Hypoxia, and Metabolism
  • RNA modifications and cancer
  • Cancer, Lipids, and Metabolism
  • Neonatal Respiratory Health Research
  • Enzyme Structure and Function
  • Antibiotic Resistance in Bacteria
  • Advanced Biosensing Techniques and Applications
  • Inhalation and Respiratory Drug Delivery
  • Ferroptosis and cancer prognosis
  • Colorectal Cancer Surgical Treatments
  • Bacteriophages and microbial interactions
  • Bacterial Genetics and Biotechnology
  • Metabolomics and Mass Spectrometry Studies
  • Telomeres, Telomerase, and Senescence
  • Cancer Cells and Metastasis
  • Peroxisome Proliferator-Activated Receptors
  • Cancer Mechanisms and Therapy
  • Cytomegalovirus and herpesvirus research
  • Systemic Sclerosis and Related Diseases
  • IL-33, ST2, and ILC Pathways
  • Pancreatic function and diabetes

Brigham and Women's Hospital
2014-2024

Joint Center for Structural Genomics
2022

Duke University Hospital
2017-2020

Duke Medical Center
2017-2020

Dana-Farber Cancer Institute
2007-2014

Dana-Farber Brigham Cancer Center
2014

Harvard University
2007-2013

Abstract Cancer cells may overcome growth factor dependence by deregulating oncogenic and/or tumor-suppressor pathways that affect their metabolism, or activating metabolic de novo with targeted mutations in critical enzymes. It is unknown whether human prostate tumors develop a similar response to different drivers particular event results its own reprogramming. Akt and Myc are arguably the most prevalent driving oncogenes cancer. Mass spectrometry–based metabolite profiling was performed...

10.1158/0008-5472.can-14-1490 article EN Cancer Research 2014-10-17

Collagen I, the most abundant protein in humans, is ubiquitous solid tumors where it provides a rich source of exploitable metabolic fuel for cancer cells. While tumor cells were unable to exploit collagen directly, here we show they can usurp byproducts collagen-consuming tumor-associated stroma. Using genetically engineered mouse models, discovered that growth depends upon binding and uptake mediated by TEM8/ANTXR1 cell surface Tumor-associated stromal processed into glutamine, which was...

10.1038/s41467-022-34643-5 article EN cc-by Nature Communications 2022-11-18

Abstract Histidine kinases are key regulators in the bacterial two-component systems that mediate cellular response to environmental changes. The vast majority of sensor histidine belong bifunctional HisKA family, displaying both kinase and phosphatase activities toward their substrates. molecular mechanisms regulating opposing these enzymes not well understood. Through a combined NMR crystallographic study on HK853 its regulator RR468 from Thermotoga maritima , here we report pH-mediated...

10.1038/s41467-017-02310-9 article EN cc-by Nature Communications 2017-12-07

Many current genome editing technologies rely on the action of large serine integrases (LSIs) to insert gene-sized DNA sequences into genome. Bxb1 is most commonly used LSI for therapeutic efforts, including PASTE, PASSIGE and I-PGI. While demonstrated good activity in vitro cycling cells, non-dividing hepatocytes was significantly less efficient. Further, wild-type known have detectable off-target at cryptic genomic sites, which presents a potential safety risk development. To address these...

10.1101/2024.10.21.619419 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-10-21

Nutrient deprivation triggers stringent response in bacteria, allowing rapid reallocation of resources from proliferation toward stress survival. Critical to this process is the accumulation/degradation (p)ppGpp regulated by RelA/SpoT homologues. While mammalian genomes encode MESH1, a homologue bacterial hydrolase SpoT, neither nor its synthetase has been identified cells. Therefore, function MESH1 remains mystery. Here, we report that human an efficient cytosolic NADPH phosphatase,...

10.1101/325266 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2018-05-17

Cancer cells undergo profound metabolic changes as a result of either abnormal signaling pathways or mutations occurring in genes encoding enzymes. A fundamental unanswered question is whether all oncogenic drivers harness similar response each event results its own specific program. Mass spectrometry‐based metabolomics was performed on immortalized human prostate epithelial transformed by the MYC and Akt oncogenes, transgenic mice driven same oncogenes under control prostate‐specific...

10.1096/fasebj.27.1_supplement.471.9 article EN The FASEB Journal 2013-04-01
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