Audrey Kelly

ORCID: 0000-0002-6570-0062
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About
Contact & Profiles
Research Areas
  • Dermatologic Treatments and Research
  • Immune Cell Function and Interaction
  • Asthma and respiratory diseases
  • T-cell and B-cell Immunology
  • melanin and skin pigmentation
  • Epigenetics and DNA Methylation
  • Skin Protection and Aging
  • Acne and Rosacea Treatments and Effects
  • Wound Healing and Treatments
  • Cytokine Signaling Pathways and Interactions
  • Estrogen and related hormone effects
  • Protein Degradation and Inhibitors
  • Retinoids in leukemia and cellular processes
  • Vitamin D Research Studies
  • Cytomegalovirus and herpesvirus research
  • CAR-T cell therapy research
  • Body Contouring and Surgery
  • Cutaneous lymphoproliferative disorders research
  • Genetic and rare skin diseases.
  • Urticaria and Related Conditions
  • Mast cells and histamine
  • Laser Applications in Dentistry and Medicine
  • Antimicrobial Peptides and Activities
  • Genomics and Chromatin Dynamics
  • Dermatological diseases and infestations

Asthma UK
2008-2025

King's College London
2011-2025

University of Pennsylvania
2024

Wilmington University
2021

Brigham and Women's Hospital
2019

Charles R. Drew University of Medicine and Science
1986-2012

University of Manchester
1992-2011

Medical Research Council
2011

University of California, Los Angeles
1986-2009

Guy's Hospital
2005-2008

Background Alterations in the stem cell niche are likely to contribute tumorigenesis; however, concept of promoted benign tumor growth remains be explored. Here we use keloid, an exuberant fibroproliferative dermal unique human skin, as a model characterize tumor-like cells and delineate role their "pathological" development tumor. Methods Findings Subclonal assay, flow cytometric multipotent differentiation analyses demonstrate that keloid contains new population cells, named derived...

10.1371/journal.pone.0007798 article EN cc-by PLoS ONE 2009-11-10

10.1016/s0733-8635(18)30653-3 article EN Dermatologic Clinics 1988-07-01

10.1016/s0190-9622(86)70021-2 article EN Journal of the American Academy of Dermatology 1986-02-01

Highlights•Th1 genes and Th2 are associated with RNA pol II in the alternative lineage•T-bet acts to recruit Mediator SEC activate Th1 eRNAs•T-bet NF-κB-dependent P-TEFb recruitment pathways converge at enhancers•P-TEFb inhibition silences T-bet target abrogates uveitis vivoSummaryThe transcription factor directs cell differentiation, but molecular mechanisms that underlie this lineage-specific gene regulation not completely understood. Here, we show through enhancers allow of form super...

10.1016/j.celrep.2016.05.054 article EN cc-by Cell Reports 2016-06-01

Abstract The PML::RARA fusion protein is the hallmark driver of Acute Promyelocytic Leukemia (APL) and disrupts retinoic acid signaling, leading to wide-scale gene expression changes uncontrolled proliferation myeloid precursor cells. While known be recruited binding sites across genome, its impact on regulation under-explored. Using integrated multi-omics datasets, we characterize influence in an inducible cell line model APL patient ex vivo samples. We find that genes whose regulatory...

10.1038/s41467-023-36262-0 article EN cc-by Nature Communications 2023-02-09

Glucocorticoids are the mainstay of asthma therapy and mediate repression a number cytokine genes, such as Interleukin (IL)-4, -5, -13, granulocyte macrophage colony-stimulating factor (GM-CSF), which central to pathogenesis asthmatic airway inflammation. The glucocorticoid receptor (GR) mediates by diverse mechanisms. We have previously suggested that one repressive activity is direct binding GR elements within GM-CSF enhancer recognized nuclear activated T cells.activator protein 1...

10.1074/jbc.m503659200 article EN cc-by Journal of Biological Chemistry 2005-04-13

Unlike acne conglobata, cystic acne, or tropical the syndrome of acute febrile ulcerative is sudden in onset, and associated with severe ulcerations, fever, polyarthralgias. Comedo formation not pronounced. Ulcers are filled gelatinous granulation tissue. Response to curettage corticosteroid hormone therapy generally prompt, but malaise arthralgias may persist for a long time.

10.1001/archderm.1971.04000200070012 article EN Archives of Dermatology 1971-08-01

10.1016/0190-9622(95)90242-2 article EN Journal of the American Academy of Dermatology 1995-08-01

Pro-inflammatory immune responses are necessary for effective pathogen clearance, but cause severe tissue damage if not shut down in a timely manner 1,2 . Excessive complement and IFN-γ-associated known drivers of immunopathogenesis 3 among the most highly induced programs hyper-inflammatory SARS-CoV2 lung infection 4 The molecular mechanisms that govern orderly shutdown retraction these remain poorly understood. Here, we show triggers contraction IFN-γ producing CD4 + T helper (Th) 1 cell...

10.1101/2020.07.18.210161 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2020-07-19

Abstract GATA3 is as a lineage-specific transcription factor that drives the differentiation of CD4 + T helper 2 (Th2) cells, but also involved in variety processes such immune regulation, proliferation and maintenance other cell non-T lineages. Here we show mechanism utilised by cells to increase mitochondrial mass response DNA damage through actions AMPK. Activated AMPK increases expression PPARG coactivator 1 alpha ( PPARGC1A or PGC1α protein) at level translation, while enhances nuclear...

10.1038/s41467-021-23715-7 article EN cc-by Nature Communications 2021-06-07
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