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Articles by Stanley B. DeVore
Study Pierces a Mystery of Healthy Skin Barrier Formation
Our skin–the body’s largest organ–provides the first line of defense against infections and many other threats to our health. Decades of research has shown that a wide range of diseases can occur, or become worse, when the skin cannot form an effective barrier. Now, experts in human genetics and asthma research at Cincinnati Children’s report discovering a novel molecular signaling pathway that plays a crucial role in maintaining our skin barrier.
GnRH Induces Citrullination of the Cytoskeleton in Murine Gonadotrope Cells
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Progressive accumulation of hyperinflammatory NKG2Dlow NK cells in early childhood severe atopic dermatitis
Research Article SKIN INFLAMMATION David E. Ochayon https://orcid.org/0000-0002-5226-5110, Stanley B. DeVore https://orcid.org/0000-0003-1570-437X, [...] , Wan-Chi Chang https://orcid.org/0009-0004-9775-928X, Durga Krishnamurthy, [...] , Harsha Seelamneni, Brittany Grashel https://orcid.org/0000-0003-3688-7857, Daniel Spagna https://orcid.org/0009-0002-8032-5034, Sandra Andorf https://orcid.org/0000-0002-3093-2568, Lisa J. Martin https://orcid.org/0000-0001-8702-9946, [...] , Jocelyn M.
Progressive accumulation of hyperinflammatory NKG2Dlow NK cells in early childhood severe atopic dermatitis
Published In Science Immunology Volume 9 | Issue 92 February 2024 Article versions Submission history Received: 13 June 2022 Accepted: 21 December 2023 Permissions Request permissions for this article. Acknowledgments We thank the participating children and families and all of the staff involved with the MPAACH study.
CARD14 is a Novel Regulator of MYC Expression and Function in Human Keratinocytes
Skin barrier disruptions are major risk factors for atopic dermatitis (AD) and atopic march progression. We recently found that the exonic CARD14 variant rs11652075 (R820W) is associated with low epidermal expression of the barrier protein filaggrin in children with AD, and that CARD14 regulates filaggrin in a genotype-dependent fashion. This suggests the variant negatively impacts barrier function.
Progressive Accumulation of Hyperinflammatory NKG2Dlow NK Cells in Early Life Defines a Novel Endotype of Severe Atopic Dermatitis
IL-4 And IL-13 Have Distinct And Overlapping Effects On Key Cell Types Involved In The Pathobiology Of Atopic Dermatitis
The role of the CBM complex in allergic inflammation and disease
Burks A.W. Holgate S.T. O’Hehir R.E. Broide D.H. Bacharier L.B. Hershey G.K.K. et al. Middleton’s allergy: principles and practice. 2020. Accessed March 25, 2020. Akdis C.A. Arkwright P.D. Brüggen M.C. Busse W. Gadina M. Guttman-Yassky E. et al. Type 2 immunity in the skin and lungs. Allergy. 2020; 75: 1582-1605 Davidson W.F. Leung D.Y.M. Beck L.A. Berin C.M. Boguniewicz M. Busse W.W. et al.
Multiancestral polygenic risk score for pediatric asthma
Footnotes Financial Disclosure R01 HG010730, R01 NS099068, R01 GM055479, U01 AI130830, R01 AI141569, and U01 AI150748 to MTW; R01 DK107502, R01 AI148276, U19 AI070235, U01 HG011172, and P30 AR070549 to LCK R01 AR073228, R01 AI024717, and CCHMC ARC Award 53632 to MTW and LCK R01 HG010166, R01 HL145422, R25 GM129808, R01 AI127392, UG3 OD023282, U19 AI070235, U54 AI117804, R01 NS096053, R01 DK107502, R01 HD089458, R01 HL132153, R01 AI139126, R01 HL135114, R01 HD099775, U01 HG011172 to LJM; R01...
The CARD14 Variant Rs11652075 Interacts with Vitamin D3 to Confer Barrier Dysfunction and Atopic Dermatitis Risk
Stanley DeVore, MS Matthew Schuetz, BS Melissa MacDonald, BS Arjun Kothari, MS Brittany Grashel, BS Elisabet Johansson, PhD Hua He, MS Jocelyn Biagini, PhD John Kroner, MS Lisa Martin, PhD Gurjit Khurana Hershey, MD PhD FAAAAI DOI:https://doi.org/10.1016/j.jaci.2021.12.497 A disrupted skin barrier is a major risk factor for the development of atopic dermatitis (AD) and progression of the atopic march.
Novel Role for Caspase Recruitment Domain Family Member 14 and its Genetic Variant rs11652075 in Skin Filaggrin Homeostasis
This paper is only available as a PDF. To read, Please Download here. Abstract Background Low epidermal filaggrin (FLG) is a risk factor for atopic dermatitis (AD) and allergic co-morbidity. FLG mutations do not fully explain the variation in epidermal FLG levels, highlighting that other genetic loci may also regulate FLG expression. Objective To identify genetic loci that regulate FLG expression and elucidate their functional and mechanistic consequences.
CARD14 is Required for FLG Homeostasis in Human Skin, and the CARD14 Variant Rs11652075 Regulates the Expression of FLG in a Genotype-Dependent Fashion
Stanley DeVore Mariana Stevens, PhD Hua He, MS Jocelyn Biagini Myers, PhD John Kroner, MS Lisa Martin, PhD Gurjit Khurana Hershey, MD PhD FAAAAI DOI:https://doi.org/10.1016/j.jaci.2020.12.551 Low epidermal filaggrin (FLG) is a major risk factor for the development and progression of atopic dermatitis (AD) and atopic march sequelae. We recently found that low non-lesional, but not lesional, FLG levels are associated with the development of co-sensitization and food allergy.
On the Surface: Skin Microbial Exposure Contributes to Allergic Disease
Burks AW, Holgate ST, O'Hehir RE, et al. Middleton's allergy: principles and practice. 2020. Oh J. Byrd A.L. Deming C. et al. Biogeography and individuality shape function in the human skin metagenome. Nature. 2014; 514: 59-64 Cundell A.M. Microbial Ecology of the Human Skin. Microb Ecol. 2018; 76: 113-120 Capone K.A. Dowd S.E. Stamatas G.N. Nikolovski J. Diversity of the human skin microbiome early in life. J Invest Dermatol. 2011; 131: 2026-2032 Ege M.J. Mayer M. Normand A.-C. et al.
Histone Citrullination Represses MicroRNA Expression, Resulting in Increased Oncogene mRNAs in Somatolactotrope Cells
Histone Citrullination Represses MicroRNA Expression, Resulting in Increased Oncogene mRNAs in Somatolactotrope Cells Stanley B. DeVore, Coleman H. Young, Guangyuan Li, Anitha Sundararajan, Thiruvarangan Ramaraj, Joann Mudge, Faye Schilkey, Aaron Muth, Paul R. Thompson, Brian D. Cherrington Molecular and Cellular Biology Sep 2018, 38 (19) e00084-18; DOI: 10.1128/MCB.00084-18
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