C
Christina A. Young
Researcher at University of Maryland, Baltimore
Publications - 8
Citations - 174
Christina A. Young is an academic researcher from University of Maryland, Baltimore. The author has contributed to research in topics: Filaggrin & Transcription factor. The author has an hindex of 5, co-authored 6 publications receiving 130 citations.
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Journal ArticleDOI
AP1 transcription factors in epidermal differentiation and skin cancer.
Richard L. Eckert,Gautam Adhikary,Christina A. Young,Ralph Jans,James F. Crish,Wen Xu,Ellen A. Rorke +6 more
TL;DR: It is suggested that individual AP1 transcription factors have different functions in the epidermis and in cancer development and that alteringAP1 transcription factor function in the basal versus suprabasal layers differentially influences theEpidermal differentiation response and disease and cancer development.
Journal ArticleDOI
Magnesium Sulfate Protects Against the Bioenergetic Consequences of Chronic Glutamate Receptor Stimulation
Pascaline Clerc,Christina A. Young,Evan A. Bordt,Alina M. Grigore,Gary Fiskum,Brian M. Polster +5 more
TL;DR: Results indicate that MgSO4 protects against chronic moderate glutamate receptor stimulation and preserves cellular ATP following treatment with excitotoxic glutamate.
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Structural and biochemical changes underlying a keratoderma-like phenotype in mice lacking suprabasal AP1 transcription factor function
Ellen A. Rorke,Gautam Adhikary,Christina A. Young,Robert H. Rice,Peter M. Elias,Debra Crumrine,Jason M. Meyer,Miroslav Blumenberg,Richard L. Eckert +8 more
TL;DR: It is suggested that AP1 factor inactivation in the suprabasal epidermal layers reduces expression ofAP1 factor-responsive genes expressed in late differentiation and is associated with a compensatory increase in expression of early differentiation genes.
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Loss of epidermal AP1 transcription factor function reduces filaggrin level, alters chemokine expression and produces an ichthyosis-related phenotype
TL;DR: It is suggested that interfering with epidermal AP1 factor signaling initiates a loss of barrier function leading to enhancedEpidermal chemokine production, but that CXCR3 and S100A8/A9 do not mediate the phenotypic response.
Journal ArticleDOI
Suppressing AP1 factor signaling in the suprabasal epidermis produces a keratoderma phenotype.
TL;DR: It is suggested that suppression of AP1 factor signaling in the suprabasal epidermis is a key event in the pathogenesis of keratoderma, and features of this phenotype are characteristic of the Vohwinkel syndrome.