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622 Regulation of XPC binding dynamics and global nucleotide excision repair by p63 and vitamin D receptor
p63 and the vitamin D receptor (VDR) play important roles in epidermal development and differentiation, but their roles and relationship in the response to ultraviolet (UV) radiation are unclear. Using TERT-immortalized human keratinocytes expressing shRNA targeting p63 in concert with exogenously applied siRNA targeting VDR, we assessed p63 and VDR ’s separate and combined effect on nucleotide excision repair (NER) of UV-induced 6-4 photoproducts (6-4PP) with a focus on the XPC DNA damage recognition protein.
Source: Journal of Investigative Dermatology - July 20, 2022 Category: Dermatology Authors: C. Wong, D.H. Oh Source Type: research

Vitamin D receptor promotes global nucleotide excision repair by facilitating XPC dissociation from damaged DNA
Vitamin D receptor (VDR) is important for normal DNA repair though the mechanism by which it acts is unclear. Following focal ultraviolet irradiation to create subnuclear spots of DNA damage, epidermal keratinocytes from VDR-null mice as well as human epidermal keratinocytes depleted of VDR with siRNA removed pyrimidine(6-4)pyrimidone photoproducts more slowly than control cells. Co-staining with antibodies to XPC, the DNA damage recognition sensor which initiates nucleotide excision repair, revealed that XPC rapidly accumulated at spots of damage and gradually faded in control human keratinocytes.
Source: Journal of Investigative Dermatology - January 28, 2021 Category: Dermatology Authors: Christian T. Wong, Dennis H. Oh Tags: Original Article Source Type: research

643 XPC dissociation from damaged DNA and efficient global nucleotide excision repair depend on vitamin D receptor
Vitamin D and its receptor, VDR, together and independently, have been associated with DNA repair, though the mechanism by which they act is unclear. Upon ultraviolet irradiation through 3 mm pores in otherwise opaque filters to create focal spots of DNA damage, epidermal keratinocytes from both VDR-null mice and human keratinocytes depleted of VDR with siRNA exhibited slower removal of 6-4 photoproducts than normal control cells over 90 minutes. Co-staining with antibodies to XPC, the initial UV-induced DNA damage recognition sensor, revealed that XPC rapidly accumulated at DNA damage foci and gradually faded over 90 minu...
Source: Journal of Investigative Dermatology - June 17, 2020 Category: Dermatology Authors: C. Wong, D.H. Oh Tags: Photobiology Source Type: research

053 Molecular mechanism of miR-145/Smad3 pathway mediated by active vitamin D in Lupus Nephritis
To elucidate the roles of 1,25(OH)2D3 and VDR in the pathogenesis of Lupus Nephritis (LN) by regulating miR-145 expression through TGF- β1-dependent Smad3 signaling pathway.From January 1, 2012 to January 1, 2017, 49 children (11 males and 38 females) with LN and 50 healthy controls were selected in this study. CD4+Tcells treated with different concentrations of 1,25(OH)2D3(1×10-6mmol/L,1×10-7mmol/L,1×10-8mmol/L).VDR-siRNA inter ference vector and human VDR overexpression vector were constructed. CD4+T cells in logarithmic growth phase were divided into 6 groups: the normal control group, the normal negative control (N...
Source: Journal of Investigative Dermatology - April 19, 2019 Category: Dermatology Authors: Y. Ding, X. He Tags: Adaptive and Auto-Immunity Source Type: research

1173 Inducible DNA repair of UV photoproducts depends on vitamin D receptor
Ultraviolet radiation (UV) initiates vitamin D synthesis by converting 7-dehydrocholesterol to pre-vitamin D3 that is converted to 25-hydroxyvitamin D3 (25D3) and then 1,25-dihydroxyvitamin D3 (1,25D3). However, UV also generates DNA damage that is repaired by nucleotide excision repair (NER). We tested the hypothesis that vitamin D signaling elicits compensatory responses to the DNA damage incurred during vitamin D synthesis. Treatment of human keratinocytes with either UVB or with 1,25D3 or 25D3 induced the DNA damage recognition protein, XPC, and induction was suppressed by either siRNA targeting the vitamin D receptor ...
Source: Journal of Investigative Dermatology - April 27, 2018 Category: Dermatology Authors: A. Scandurra, C. Wong, T. Kaur Oberoi, D. Oh Tags: Photobiology Source Type: research

310 Sphingosine-1-phosphate stimulates CAMP expression through a novel stress specific signaling complex formation
We recently discovered a novel sphingosine-1-phosphate (S1P)-induced signaling mechanism of cathelicidin antimicrobial peptide (CAMP) production in response to external perturbant-mediated endoplasmic reticulum (ER) stress. Activation occurs by an S1P receptor (S1PR)–independent activation of NF-κB, followed by C/EBPα transactivation (rather than through the well-established vitamin D receptor-mediated mechanism). Yet, how S1P activates NF-κB remains unresolved. In addition to using both specific activators and inhibitors of each S1PR isomers, we have employed a gene silencing approach and showed that ER stress-induce...
Source: Journal of Investigative Dermatology - April 20, 2016 Category: Dermatology Authors: K. Park, H. Ikushiro, H. Seo, K. Shin, T. Yano, W.M. Holleran, P.M. Elias, Y. Uchida Tags: Epidermal Structure & Barrier Function Source Type: research