Structure Composition and Intracellular Transport of Clathrin-Mediated Intestinal Transmembrane Tight Junction Protein

Pan, Yi-Yang; Deng, Ying; Su, Shuai; Yin, Jiuheng; Chen, Yihui; Wang, Liu-Can; Sun, Ling; Xiao, Weidong; Du, Guangsheng

doi:10.1007/s10753-022-01724-y

Cited by 7 publications

(2 citation statements)

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“…6 Therefore, normal tight junction structure, including tight junction family proteins and proteins associated with tight junctions, is essential for maintaining skin barrier function and immune homeostasis. 7,8 External environmental factors, such as substances (caused by ultraviolet light [UV]), allergens and microorganisms, are readily able to pass through damaged tight junctions. These substances can be recognized by Langerhans cells and then presented to T cells, causing delayed hypersensitivity.…”

Section: Introductionmentioning

confidence: 99%

“…As well, epicutaneous application of CLDN1 TJ‐interfering peptides could promote the immune response of mice after disrupting TJ in mouse skin 6 . Therefore, normal tight junction structure, including tight junction family proteins and proteins associated with tight junctions, is essential for maintaining skin barrier function and immune homeostasis 7,8 …”

Section: Introductionmentioning

confidence: 99%

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LncRNA‐WAKMAR2 regulates expression of CLDN1 to affect skin barrier through recruiting c‐Fos

Wang

et al. 2022

Contact Dermatitis

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Background: Chronic actinic dermatitis (CAD) is an immune-mediated photo-allergic skin disease. In the clinic, the treatment of this disease is hampered by the lack of proper understanding of the skin barrier dysfunction mechanism.Objective: To illuminate the mechanism of skin barrier dysfunction in CAD.Methods: Transcriptome sequencing and protein profiling were used to detect skin barrier injury-related genes. RNA pull down, a promoter-reporter gene assay, and chromatin isolation by RNA purification-sequencing were used to elucidate the effect of WAKMAR2 in skin barrier functionality.Results: Transcriptome sequencing from patient's tissues showed a significantly decreased expression of WAKMAR2. Down-regulation of WAKMAR2 destroyed the keratinocyte barrier. Moreover, WAKMAR2 can directly bind to the c-Fos protein.This novel long non-coding RNA (LncRNA)-protein complexes were targeted to the CLDN1 promotor. Overexpression of WAKMAR2 enhanced the promoter activity of CLDN1, while the addition of AP-1 inhibitor could reverse this phenomenon. Furthermore, our in vivo results suggested that expression of WAKMAR2 was required for the repair of skin damage in mice induced by ultraviolet irradiation. Conclusions:We identified a crucial LncRNA (WAKMAR2) for the protection of the skin barrier in vitro and in vivo. Mechanically, it can specifically interact with c-Fos protein for the regulation of CLDN1, a finding which could be applied for CAD treatment.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%