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Corrections to “Melanocyte and Keratinocyte Carcinogenesis: p53 Family Protein Activities and Intersecting mRNA Expression Profiles”

        Correction to: Journal of Investigative Dermatology Symposium Proceedings (2005) 10, 142–52. doi:10.111/j.1087-0024.2005.200405.x
        In the publication by Kulesz-Martin et al., the authors reported that the TAp63α isoform was expressed in a keratinocyte model system in vitro, based upon reverse transcription-PCR analysis. We have since confirmed by immunoblotting using isoform-specific antibodies (provided by Dr Wendy Weinberg) and comparison with known molecular weight p63 isoforms ectopically expressed in keratinocytes that the TAp63α isoform is not expressed in the keratinocyte model but that the p63 isoforms present are identical to those in primary keratinocyte cultures. Thus, the p53 family members in keratinocytes are as follows in order of apparent molecular weight from greatest to least: ΔNp63α, TAp63β, TAp63γ, and either ΔNp63γ or ΔNp63s with ΔNp63α predominating. In the melanocyte model, the p63 isoforms expressed are TAp63γ, and either ΔNp63γ or ΔNp63s with the lower molecular weight isoform predominating.
        The corrected Figures 2, 3 (keratinocytes in left panel), and 5 (summary of changes in p53 family expressions during carcinogenesis of keratinocytes and melanocytes) are shown. All text in the paper referring to TAp63α expression in keratinocytes and melanocytes should instead read ΔNp63α and discussion of TAp63β should read TAp63γ, a more transcriptionally active p63 isoform.

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        • Melanocyte and Keratinocyte Carcinogenesis: p53 Family Protein Activities and Intersecting mRNA Expression Profiles
          Journal of Investigative Dermatology Symposium ProceedingsVol. 10Issue 2
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            Melanocytes and keratinocytes were analyzed for potential roles of p53, p73, and p63 tumor suppressor family proteins and of malignancy-specific gene expression changes in the etiology of multi-step cancer. Melanocytes expressed ΔNp73α, two p63 isoforms and p53. Although p21 and Noxa mRNA levels increased following DNA damage, p53 family member binding to p21 and Noxa DNA probes was undetectable, suggesting p53 family-independent responses. In contrast, keratinocytes expressed multiple isoforms each of p73 and p63 that were induced to bind p21 and Noxa DNA probes after ionizing (IR) or after ultraviolet B (UVB) irradiation, correlating with p21 and Noxa mRNA induction and with apoptosis.
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