Shane J. F. Cronin

ORCID: 0000-0003-4222-5315
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About
Contact & Profiles
Research Areas
  • Pain Mechanisms and Treatments
  • Bone Metabolism and Diseases
  • Epigenetics and DNA Methylation
  • RNA modifications and cancer
  • Diet and metabolism studies
  • Neurobiology and Insect Physiology Research
  • Bone health and treatments
  • Neuropeptides and Animal Physiology
  • Parkinson's Disease Mechanisms and Treatments
  • Cell death mechanisms and regulation
  • Cytokine Signaling Pathways and Interactions
  • Melanoma and MAPK Pathways
  • Pancreatic function and diabetes
  • Cancer-related gene regulation
  • Invertebrate Immune Response Mechanisms
  • CAR-T cell therapy research
  • Adipose Tissue and Metabolism
  • Immune Cell Function and Interaction
  • Signaling Pathways in Disease
  • Pharmacological Effects of Natural Compounds
  • Plant Toxicity and Pharmacological Properties
  • TGF-β signaling in diseases
  • Synthesis of Tetrazole Derivatives
  • Pain Management and Opioid Use
  • T-cell and B-cell Immunology

AstraZeneca (United States)
2025

Medical University of Vienna
2024

Austrian Academy of Sciences
2014-2024

Institute of Molecular Biotechnology
2014-2024

Boston Children's Hospital
2013-2023

Harvard University
2015-2023

Vienna Biocenter
2017-2020

Boston University
2013

Scripps Research Institute
2012

Massey University
2007

Innate Immunity in the Fly Gut Drosophila melanogaster is an important model system to study innate immunity, being both easy manipulate and lacking adaptive immune system. In order identify genes that regulate Cronin et al. (p. 340 ; published online 11 June) performed RNA interference screen on flies infected with oral bacterial pathogen, Serratia marcescens . Genes involved intestinal immunity regulation of hemocytes, macrophage-like cells critical for phagocytosis killing bacteria, were...

10.1126/science.1173164 article EN Science 2009-06-12

Abstract Type 2 diabetes mellitus is one of the most prevalent metabolic diseases presenting with systemic pathologies, including reproductive disorders in male diabetic patients. However, molecular mechanisms that contributing to spermatogenesis dysfunction patients have not yet been fully elucidated. Here, we perform STRT-seq examine transcriptome patients’ testes at single-cell resolution all major cell types testis. Intriguingly, whereas appears largely preserved, gene expression...

10.1038/s41467-022-34990-3 article EN cc-by Nature Communications 2022-11-28

Increased tetrahydrobiopterin (BH4) generated in injured sensory neurons contributes to increased pain sensitivity and its persistence. GTP cyclohydrolase 1 (GCH1) is the rate-limiting enzyme de novo BH4 synthetic pathway, human single-nucleotide polymorphism studies, together with mouse genetic modeling, have demonstrated that decreased GCH1 leads both reduced pain. However, little known about regulation of Gch1 expression upon nerve injury whether this could be modulated as an analgesic...

10.1126/scitranslmed.abj1531 article EN Science Translational Medicine 2022-08-31

Postoperative pain affects most patients after major surgery and can transition to chronic pain. The considerable side effects limited efficacy of current treatments underline the need for new therapeutic options. We observed increased amounts metabolites BH4 serotonin skin injury. Mast cells were primary postoperative sources Gch1 , rate-limiting enzyme in synthesis, itself an obligate cofactor production by tryptophan hydroxylase (Tph1). Mice deficient mast or cell–specific Tph1 showed...

10.1126/sciimmunol.adh0545 article EN Science Immunology 2024-08-23

Abstract Apoptosis inducing factor (AIF) has been shown to be a major contributor neuron loss in the immature brain after hypoxia-ischemia (HI). Indeed, mice bearing hypomorphic mutation causing reduced AIF expression are protected against neonatal HI. To further investigate possible molecular mechanisms of this neuroprotection, we generated an knock-in mouse by introduction latent transgene coding for flagged protein into Rosa26 locus, followed its conditional activation ubiquitously...

10.1038/s41419-020-2280-z article EN cc-by Cell Death and Disease 2020-01-30

Abstract Elevated expression of folate receptor alpha (FRα) in various cancers, including epithelial ovarian cancer (EOC), highlights FRα as a potential target for the development novel therapeutics to treat FRα-expressing tumor types. AZD5335, an FRα-targeting antibody conjugated topoisomerase 1 inhibitor (TOP1i) payload, is currently being investigated FONTANA Phase I/IIa clinical trial (NCT#05797168), either single agent or combination with PARP1-selective (saruparib). Using EOC xenograft...

10.1158/1538-7445.am2025-815 article EN Cancer Research 2025-04-21

Lung cancer is the leading cause of deaths. Besides smoking, epidemiological studies have linked female sex hormones to lung in women; however, underlying mechanisms remain unclear. Here we report that receptor activator nuclear factor-kB (RANK), key regulator osteoclastogenesis, frequently expressed primary tumors, an active RANK pathway correlates with decreased survival, and pharmacologic inhibition reduces tumor growth patient-derived xenografts. Clonal genetic inactivation KRasG12D...

10.1101/gad.304162.117 article EN Genes & Development 2017-10-15

The HUSH (human silencing hub) complex contains the H3K9me3 binding protein M-phase phosphoprotein 8 (MPP8) and recruits histone methyltransferase SETDB1 as well Microrchidia CW-type zinc finger 2 (MORC2). Functional mechanistic studies of have hitherto been centered around while in vivo functions MPP8 MORC2 remain elusive. Here, we show that genetic inactivation Mphosph8 or Morc2a nervous system mice leads to increased brain size, altered architecture, behavioral changes. Mechanistically,...

10.1126/sciadv.abo7247 article EN cc-by-nc Science Advances 2022-11-04

The protein kinase MKK7 is linked to neuronal development and the onset of cancer. field, however, lacks high-quality functional probes that would allow for dissection its detailed functions. Against this background, we describe an effective covalent inhibitor based on pyrazolopyrimidine scaffold.

10.1021/acs.jmedchem.9b00102 article EN Journal of Medicinal Chemistry 2019-02-15
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