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{{Infobox_gene}}
{{Infobox_gene}}
'''Tumor protein p63''' also known as '''transformation-related protein 63''' is a [[protein]] that in humans is encoded by the '''''TP63''''' [[gene]].<ref name="pmid9774969">{{cite journal | vauthors = Yang A, Kaghad M, Wang Y, Gillett E, Fleming MD, Dötsch V, Andrews NC, Caput D, McKeon F | title = p63, a p53 homolog at 3q27-29, encodes multiple products with transactivating, death-inducing, and dominant-negative activities | journal = Molecular Cell | volume = 2 | issue = 3 | pages = 305–16 | date = Sep 1998 | pmid = 9774969 | doi = 10.1016/S1097-2765(00)80275-0 }}</ref><ref name="pmid9662378">{{cite journal | vauthors = Osada M, Ohba M, Kawahara C, Ishioka C, Kanamaru R, Katoh I, Ikawa Y, Nimura Y, Nakagawara A, Obinata M, Ikawa S | title = Cloning and functional analysis of human p51, which structurally and functionally resembles p53 | journal = Nature Medicine | volume = 4 | issue = 7 | pages = 839–43 | date = Jul 1998 | pmid = 9662378 | doi = 10.1038/nm0798-839 }}</ref><ref name="pmid11181441">{{cite journal | vauthors = Zeng X, Zhu Y, Lu H | title = NBP is the p53 homolog p63 | journal = Carcinogenesis | volume = 22 | issue = 2 | pages = 215–9 | date = Feb 2001 | pmid = 11181441 | doi = 10.1093/carcin/22.2.215 }}</ref><ref name="pmid11181451">{{cite journal | vauthors = Tan M, Bian J, Guan K, Sun Y | title = p53CP is p51/p63, the third member of the p53 gene family: partial purification and characterization | journal = Carcinogenesis | volume = 22 | issue = 2 | pages = 295–300 | date = Feb 2001 | pmid = 11181451 | doi = 10.1093/carcin/22.2.295 }}</ref>
'''Tumor protein p63,''' typically referred to as '''p63''', also known as '''transformation-related protein 63''' is a [[protein]] that in humans is encoded by the '''''TP63''''' (also known as the ''''' p63''''') [[gene]].<ref name="pmid9774969">{{cite journal | vauthors = Yang A, Kaghad M, Wang Y, Gillett E, Fleming MD, Dötsch V, Andrews NC, Caput D, McKeon F | title = p63, a p53 homolog at 3q27-29, encodes multiple products with transactivating, death-inducing, and dominant-negative activities | journal = Molecular Cell | volume = 2 | issue = 3 | pages = 305–16 | date = Sep 1998 | pmid = 9774969 | doi = 10.1016/S1097-2765(00)80275-0 }}</ref><ref name="pmid9662378">{{cite journal | vauthors = Osada M, Ohba M, Kawahara C, Ishioka C, Kanamaru R, Katoh I, Ikawa Y, Nimura Y, Nakagawara A, Obinata M, Ikawa S | title = Cloning and functional analysis of human p51, which structurally and functionally resembles p53 | journal = Nature Medicine | volume = 4 | issue = 7 | pages = 839–43 | date = Jul 1998 | pmid = 9662378 | doi = 10.1038/nm0798-839 }}</ref><ref name="pmid11181441">{{cite journal | vauthors = Zeng X, Zhu Y, Lu H | title = NBP is the p53 homolog p63 | journal = Carcinogenesis | volume = 22 | issue = 2 | pages = 215–9 | date = Feb 2001 | pmid = 11181441 | doi = 10.1093/carcin/22.2.215 }}</ref><ref name="pmid11181451">{{cite journal | vauthors = Tan M, Bian J, Guan K, Sun Y | title = p53CP is p51/p63, the third member of the p53 gene family: partial purification and characterization | journal = Carcinogenesis | volume = 22 | issue = 2 | pages = 295–300 | date = Feb 2001 | pmid = 11181451 | doi = 10.1093/carcin/22.2.295 }}</ref>


TP63 also known as the '''p63''' gene was discovered 20 years after the discovery of the [[p53]] tumor suppressor gene and along with [[p73]] constitutes the p53 gene family based on their structural similarity.<ref name="pmid12750249">{{cite journal | vauthors = Wu G, Nomoto S, Hoque MO, Dracheva T, Osada M, Lee CC, Dong SM, Guo Z, Benoit N, Cohen Y, Rechthand P, Califano J, Moon CS, Ratovitski E, Jen J, Sidransky D, Trink B | title = DeltaNp63alpha and TAp63alpha regulate transcription of genes with distinct biological functions in cancer and development | journal = Cancer Research | volume = 63 | issue = 10 | pages = 2351–7 | date = May 2003 | pmid = 12750249 | doi =  }}</ref>  Despite being discovered significantly later than p53, phylogenetic analysis of p53, p63 and p73, suggest that p63 was the original member of the family from which p53 and p73 evolved.<ref name="Skipper_2007">{{cite journal | vauthors = Skipper M | title = Dedicated protection for the female germline | journal=Nature Reviews Molecular Cell Biology |date=January 2007 | volume = 8 | pages = 4–5 | doi = 10.1038/nrm2091 | issue=1}}</ref>
The ''TP63'' gene was discovered 20 years after the discovery of the ''[[p53]]'' tumor suppressor gene and along with ''[[p73]]'' constitutes the ''p53'' gene family based on their structural similarity.<ref name="pmid12750249">{{cite journal | vauthors = Wu G, Nomoto S, Hoque MO, Dracheva T, Osada M, Lee CC, Dong SM, Guo Z, Benoit N, Cohen Y, Rechthand P, Califano J, Moon CS, Ratovitski E, Jen J, Sidransky D, Trink B | title = DeltaNp63alpha and TAp63alpha regulate transcription of genes with distinct biological functions in cancer and development | journal = Cancer Research | volume = 63 | issue = 10 | pages = 2351–7 | date = May 2003 | pmid = 12750249 | doi =  }}</ref>  Despite being discovered significantly later than ''p53'', phylogenetic analysis of ''p53'', ''p63'' and ''p73'', suggest that ''p63'' was the original member of the family from which ''p53'' and ''p73'' evolved.<ref name="Skipper_2007">{{cite journal | vauthors = Skipper M | title = Dedicated protection for the female germline | journal=Nature Reviews Molecular Cell Biology |date=January 2007 | volume = 8 | pages = 4–5 | doi = 10.1038/nrm2091 | issue=1}}</ref>


== Function ==
== Function ==
Tumor protein p63 is a member of the p53 family of [[transcription factor]]s. p63 -/- mice have several developmental defects which include the lack of limbs and other tissues, such as teeth and mammary glands, which develop as a result of interactions between [[mesenchyme]] and [[epithelium]]. TP63 encodes for two main isoforms by alternative promoters (TAp63 and ΔNp63). ΔNp63 is involved in multiple functions during skin development and in adult stem/progenitor cell regulation.<ref name="pmid20078223">{{cite journal | vauthors = Crum CP, McKeon FD | title = p63 in epithelial survival, germ cell surveillance, and neoplasia | journal = Annual Review of Pathology | volume = 5 | issue =  | pages = 349–71 | year = 2010 | pmid = 20078223 | doi = 10.1146/annurev-pathol-121808-102117 }}</ref> In contrast, TAp63 has been mostly restricted to its apoptotic function and more recently as the guardian of oocyte integrity.<ref name="pmid21335238">{{cite journal | vauthors = Deutsch GB, Zielonka EM, Coutandin D, Weber TA, Schäfer B, Hannewald J, Luh LM, Durst FG, Ibrahim M, Hoffmann J, Niesen FH, Sentürk A, Kunkel H, Brutschy B, Schleiff E, Knapp S, Acker-Palmer A, Grez M, McKeon F, Dötsch V | title = DNA damage in oocytes induces a switch of the quality control factor TAp63α from dimer to tetramer | journal = Cell | volume = 144 | issue = 4 | pages = 566–76 | date = Feb 2011 | pmid = 21335238 | pmc = 3087504 | doi = 10.1016/j.cell.2011.01.013 }}</ref> Recently, two new functions have been attributed to TAp63 in heart development<ref name="pmid21898690">{{cite journal | vauthors = Rouleau M, Medawar A, Hamon L, Shivtiel S, Wolchinsky Z, Zhou H, De Rosa L, Candi E, de la Forest Divonne S, Mikkola ML, van Bokhoven H, Missero C, Melino G, Pucéat M, Aberdam D | title = TAp63 is important for cardiac differentiation of embryonic stem cells and heart development | journal = Stem Cells | volume = 29 | issue = 11 | pages = 1672–83 | date = Nov 2011 | pmid = 21898690 | doi = 10.1002/stem.723 | url = http://minus.com/lNWTY9g2q5yYG }}</ref> and premature aging.<ref name="pmid19570515">{{cite journal | vauthors = Su X, Paris M, Gi YJ, Tsai KY, Cho MS, Lin YL, Biernaskie JA, Sinha S, Prives C, Pevny LH, Miller FD, Flores ER | title = TAp63 prevents premature aging by promoting adult stem cell maintenance | journal = Cell Stem Cell | volume = 5 | issue = 1 | pages = 64–75 | date = Jul 2009 | pmid = 19570515 | pmc = 3418222 | doi = 10.1016/j.stem.2009.04.003 }}</ref>
Tumor protein p63 is a member of the p53 family of [[transcription factor]]s. p63 -/- mice have several developmental defects which include the lack of limbs and other tissues, such as teeth and mammary glands, which develop as a result of interactions between [[mesenchyme]] and [[epithelium]]. TP63 encodes for two main isoforms by alternative promoters (TAp63 and ΔNp63). ΔNp63 is involved in multiple functions during skin development and in adult stem/progenitor cell regulation.<ref name="pmid20078223">{{cite journal | vauthors = Crum CP, McKeon FD | title = p63 in epithelial survival, germ cell surveillance, and neoplasia | journal = Annual Review of Pathology | volume = 5 | issue =  | pages = 349–71 | year = 2010 | pmid = 20078223 | doi = 10.1146/annurev-pathol-121808-102117 }}</ref> In contrast, TAp63 has been mostly restricted to its apoptotic function and more recently as the guardian of oocyte integrity.<ref name="pmid21335238">{{cite journal | vauthors = Deutsch GB, Zielonka EM, Coutandin D, Weber TA, Schäfer B, Hannewald J, Luh LM, Durst FG, Ibrahim M, Hoffmann J, Niesen FH, Sentürk A, Kunkel H, Brutschy B, Schleiff E, Knapp S, Acker-Palmer A, Grez M, McKeon F, Dötsch V | title = DNA damage in oocytes induces a switch of the quality control factor TAp63α from dimer to tetramer | journal = Cell | volume = 144 | issue = 4 | pages = 566–76 | date = Feb 2011 | pmid = 21335238 | pmc = 3087504 | doi = 10.1016/j.cell.2011.01.013 }}</ref> Recently, two new functions have been attributed to TAp63 in heart development<ref name="pmid21898690">{{cite journal | vauthors = Rouleau M, Medawar A, Hamon L, Shivtiel S, Wolchinsky Z, Zhou H, De Rosa L, Candi E, de la Forest Divonne S, Mikkola ML, van Bokhoven H, Missero C, Melino G, Pucéat M, Aberdam D | title = TAp63 is important for cardiac differentiation of embryonic stem cells and heart development | journal = Stem Cells | volume = 29 | issue = 11 | pages = 1672–83 | date = Nov 2011 | pmid = 21898690 | doi = 10.1002/stem.723 | url = http://minus.com/lNWTY9g2q5yYG | deadurl = yes | archiveurl = https://web.archive.org/web/20140808060204/http://minus.com/lNWTY9g2q5yYG | archivedate = 2014-08-08 | df =  }}</ref> and premature aging.<ref name="pmid19570515">{{cite journal | vauthors = Su X, Paris M, Gi YJ, Tsai KY, Cho MS, Lin YL, Biernaskie JA, Sinha S, Prives C, Pevny LH, Miller FD, Flores ER | title = TAp63 prevents premature aging by promoting adult stem cell maintenance | journal = Cell Stem Cell | volume = 5 | issue = 1 | pages = 64–75 | date = Jul 2009 | pmid = 19570515 | pmc = 3418222 | doi = 10.1016/j.stem.2009.04.003 }}</ref>


== Clinical significance ==
== Clinical significance ==


TP63 mutations underlie several malformation syndromes that include cleft lip and/or palate as a hallmark feature.<ref name="Dixon_2011"/> Mutations in the TP63 gene are associated with [[ectrodactyly-ectodermal dysplasia-cleft syndrome]] in which a midline cleft lip is a common feature,<ref name="Dixon_2011">{{cite journal | vauthors = Dixon MJ, Marazita ML, Beaty TH, Murray JC | title = Cleft lip and palate: understanding genetic and environmental influences | journal = Nature Reviews Genetics | volume = 12 | issue = 3 | pages = 167–78 | date = Mar 2011 | pmid = 21331089 | pmc = 3086810 | doi = 10.1038/nrg2933 }}</ref> [[cleft lip/palate syndrome 3]] (EEC3); [[ectrodactyly]] (also known as split-hand/foot malformation 4 (SHFM4)); ankyloblepharon-ectodermal dysplasia-cleft lip/palate (AEC) or [[Hay–Wells syndrome]] in which a midline cleft lip is also a common feature,<ref name="Dixon_2011" /> [[Acro–dermato–ungual–lacrimal–tooth syndrome]] (ADULT); [[limb-mammary syndrome]]; [[Rap-Hodgkin syndrome]] (RHS); and [[orofacial cleft]] 8. Both cleft lip with or without a cleft palate and cleft palate only features have been seen to segregate within the same family with a TP63 mutation.<ref name="Dixon_2011" /> Recently, induced pluripotent stem cells have been produced from patients affected by EEC syndromes by cell reprogramming. The defective epithelial commitment could be partially rescued by a small therapeutic compound.<ref>Shalom Feuerstein R. et al. Impaired epithelial differentiation of induced pluripotent stem cells from EEC patients is rescued by APR-246/PRIMA-1MET. P.N.A.S 2012. http://minus.com/lbmC3TVGDx350s</ref>
''TP63'' mutations underlie several malformation syndromes that include cleft lip and/or palate as a hallmark feature.<ref name="Dixon_2011"/> Mutations in the ''TP63'' gene are associated with [[ectrodactyly-ectodermal dysplasia-cleft syndrome]] in which a midline cleft lip is a common feature,<ref name="Dixon_2011">{{cite journal | vauthors = Dixon MJ, Marazita ML, Beaty TH, Murray JC | title = Cleft lip and palate: understanding genetic and environmental influences | journal = Nature Reviews Genetics | volume = 12 | issue = 3 | pages = 167–78 | date = Mar 2011 | pmid = 21331089 | pmc = 3086810 | doi = 10.1038/nrg2933 }}</ref> [[cleft lip/palate syndrome 3]] (EEC3); [[ectrodactyly]] (also known as split-hand/foot malformation 4 (SHFM4)); ankyloblepharon-ectodermal dysplasia-cleft lip/palate (AEC) or [[Hay–Wells syndrome]] in which a midline cleft lip is also a common feature,<ref name="Dixon_2011" /> [[Acro–dermato–ungual–lacrimal–tooth syndrome]] (ADULT); [[limb-mammary syndrome]]; [[Rap-Hodgkin syndrome]] (RHS); and [[orofacial cleft]] 8.  
 
[[File:P63 staining on prostate cancer tissue using antibody clone IHC063.jpg|thumb|p63 staining on prostate cancer tissue using antibody clone IHC063]]
 
Both cleft lip with or without a cleft palate and cleft palate only features have been seen to segregate within the same family with a ''TP63'' mutation.<ref name="Dixon_2011" /> Recently, induced pluripotent stem cells have been produced from patients affected by EEC syndromes by cell reprogramming. The defective epithelial commitment could be partially rescued by a small therapeutic compound.<<ref name="pmid23355677">{{cite journal | vauthors = Shalom-Feuerstein R, Serror L, Aberdam E, Müller FJ, van Bokhoven H, Wiman KG, Zhou H, Aberdam D, Petit I | display-authors = 6 | title = Impaired epithelial differentiation of induced pluripotent stem cells from ectodermal dysplasia-related patients is rescued by the small compound APR-246/PRIMA-1MET | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 110 | issue = 6 | pages = 2152–6 | date = February 2013 | pmid = 23355677 | pmc = 3568301 | doi = 10.1073/pnas.1201753109 }}</ref>


== Diagnostic utility ==
== Diagnostic utility ==
Line 21: Line 25:
==Regulation==
==Regulation==


There is some evidence that the expression of p63 is regulated by the microRNA [[Mir-203 microRNA|miR-203]].<ref name="pmid18311128">{{cite journal | vauthors = Yi R, Poy MN, Stoffel M, Fuchs E | title = A skin microRNA promotes differentiation by repressing 'stemness' | journal = Nature | volume = 452 | issue = 7184 | pages = 225–9 | date = Mar 2008 | pmid = 18311128 | doi = 10.1038/nature06642 }}</ref><ref name="pmid18848452">{{cite journal | vauthors = Aberdam D, Candi E, Knight RA, Melino G | title = miRNAs, 'stemness' and skin | journal = Trends in Biochemical Sciences | volume = 33 | issue = 12 | pages = 583–91 | date = Dec 2008 | pmid = 18848452 | doi = 10.1016/j.tibs.2008.09.002 | url = http://min.us/lGvvAc29SY8ux }}</ref>
There is some evidence that the expression of p63 is regulated by the microRNA [[Mir-203 microRNA|miR-203]].<ref name="pmid18311128">{{cite journal | vauthors = Yi R, Poy MN, Stoffel M, Fuchs E | title = A skin microRNA promotes differentiation by repressing 'stemness' | journal = Nature | volume = 452 | issue = 7184 | pages = 225–9 | date = Mar 2008 | pmid = 18311128 | doi = 10.1038/nature06642 | pmc = 4346711 }}</ref><ref name="pmid18848452">{{cite journal | vauthors = Aberdam D, Candi E, Knight RA, Melino G | title = miRNAs, 'stemness' and skin | journal = Trends in Biochemical Sciences | volume = 33 | issue = 12 | pages = 583–91 | date = Dec 2008 | pmid = 18848452 | doi = 10.1016/j.tibs.2008.09.002 | url = http://min.us/lGvvAc29SY8ux | archive-url = https://archive.is/20130421181244/http://min.us/lGvvAc29SY8ux | dead-url = yes | archive-date = 2013-04-21 }}</ref>


== See also ==
== See also ==
Line 46: Line 50:
* {{MeshName|TP73L+protein,+human}}
* {{MeshName|TP73L+protein,+human}}
* [https://www.ncbi.nlm.nih.gov/books/NBK43797/  GeneReviews/NCBI/NIH/UW entry on Ankyloblepharon-Ectodermal Defects-Cleft Lip/Palate Syndrome or AEC Syndrome, Hay-Wells Syndrome. Includes: Rapp-Hodgkin Syndrome]
* [https://www.ncbi.nlm.nih.gov/books/NBK43797/  GeneReviews/NCBI/NIH/UW entry on Ankyloblepharon-Ectodermal Defects-Cleft Lip/Palate Syndrome or AEC Syndrome, Hay-Wells Syndrome. Includes: Rapp-Hodgkin Syndrome]
* [https://www.ncbi.nlm.nih.gov/omim/106260,603273,106260,603273 OMIM entries on AEC]
* [https://www.ncbi.nlm.nih.gov/omim/106260,603273,106260,603273 OMIM entries on AEC]
* {{UCSC genome browser|TP63}}
* {{UCSC genome browser|TP63}}
* {{UCSC gene details|TP63}}
* {{UCSC gene details|TP63}}

Latest revision as of 06:11, 17 January 2019

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SpeciesHumanMouse
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View/Edit Human

Tumor protein p63, typically referred to as p63, also known as transformation-related protein 63 is a protein that in humans is encoded by the TP63 (also known as the p63) gene.[1][2][3][4]

The TP63 gene was discovered 20 years after the discovery of the p53 tumor suppressor gene and along with p73 constitutes the p53 gene family based on their structural similarity.[5] Despite being discovered significantly later than p53, phylogenetic analysis of p53, p63 and p73, suggest that p63 was the original member of the family from which p53 and p73 evolved.[6]

Function

Tumor protein p63 is a member of the p53 family of transcription factors. p63 -/- mice have several developmental defects which include the lack of limbs and other tissues, such as teeth and mammary glands, which develop as a result of interactions between mesenchyme and epithelium. TP63 encodes for two main isoforms by alternative promoters (TAp63 and ΔNp63). ΔNp63 is involved in multiple functions during skin development and in adult stem/progenitor cell regulation.[7] In contrast, TAp63 has been mostly restricted to its apoptotic function and more recently as the guardian of oocyte integrity.[8] Recently, two new functions have been attributed to TAp63 in heart development[9] and premature aging.[10]

Clinical significance

TP63 mutations underlie several malformation syndromes that include cleft lip and/or palate as a hallmark feature.[11] Mutations in the TP63 gene are associated with ectrodactyly-ectodermal dysplasia-cleft syndrome in which a midline cleft lip is a common feature,[11] cleft lip/palate syndrome 3 (EEC3); ectrodactyly (also known as split-hand/foot malformation 4 (SHFM4)); ankyloblepharon-ectodermal dysplasia-cleft lip/palate (AEC) or Hay–Wells syndrome in which a midline cleft lip is also a common feature,[11] Acro–dermato–ungual–lacrimal–tooth syndrome (ADULT); limb-mammary syndrome; Rap-Hodgkin syndrome (RHS); and orofacial cleft 8.

File:P63 staining on prostate cancer tissue using antibody clone IHC063.jpg
p63 staining on prostate cancer tissue using antibody clone IHC063

Both cleft lip with or without a cleft palate and cleft palate only features have been seen to segregate within the same family with a TP63 mutation.[11] Recently, induced pluripotent stem cells have been produced from patients affected by EEC syndromes by cell reprogramming. The defective epithelial commitment could be partially rescued by a small therapeutic compound.<[12]

Diagnostic utility

p63 immunostaining has utility for head and neck squamous cell carcinomas, differentiating prostatic adenocarcinoma (the most common type of prostate cancer) and benign prostatic tissue;[13] normal prostatic glands stain with p63 (as they have basal cells), while the malignant glands in prostatic adenocarcinoma (which lacks these cells) do not.[14] P63 is also helpful in distinguishing poorly differentiated squamous cell carcinoma from small cell carcinoma or adenocarcinoma. P63 should be strongly stained in poorly differentiated squamous cell, but negative in small cell or adenocarcinoma.[15]

Interactions

TP63 has been shown to interact with HNRPAB.[16] It also activates IRF6 transcription through the IRF6 enhancer element.[11]

Regulation

There is some evidence that the expression of p63 is regulated by the microRNA miR-203.[17][18]

See also

  • AMACR - another marker for prostate adenocarcinoma

References

  1. ↑ Yang A, Kaghad M, Wang Y, Gillett E, Fleming MD, Dötsch V, Andrews NC, Caput D, McKeon F (Sep 1998). "p63, a p53 homolog at 3q27-29, encodes multiple products with transactivating, death-inducing, and dominant-negative activities". Molecular Cell. 2 (3): 305–16. doi:10.1016/S1097-2765(00)80275-0. PMID 9774969.
  2. ↑ Osada M, Ohba M, Kawahara C, Ishioka C, Kanamaru R, Katoh I, Ikawa Y, Nimura Y, Nakagawara A, Obinata M, Ikawa S (Jul 1998). "Cloning and functional analysis of human p51, which structurally and functionally resembles p53". Nature Medicine. 4 (7): 839–43. doi:10.1038/nm0798-839. PMID 9662378.
  3. ↑ Zeng X, Zhu Y, Lu H (Feb 2001). "NBP is the p53 homolog p63". Carcinogenesis. 22 (2): 215–9. doi:10.1093/carcin/22.2.215. PMID 11181441.
  4. ↑ Tan M, Bian J, Guan K, Sun Y (Feb 2001). "p53CP is p51/p63, the third member of the p53 gene family: partial purification and characterization". Carcinogenesis. 22 (2): 295–300. doi:10.1093/carcin/22.2.295. PMID 11181451.
  5. ↑ Wu G, Nomoto S, Hoque MO, Dracheva T, Osada M, Lee CC, Dong SM, Guo Z, Benoit N, Cohen Y, Rechthand P, Califano J, Moon CS, Ratovitski E, Jen J, Sidransky D, Trink B (May 2003). "DeltaNp63alpha and TAp63alpha regulate transcription of genes with distinct biological functions in cancer and development". Cancer Research. 63 (10): 2351–7. PMID 12750249.
  6. ↑ Skipper M (January 2007). "Dedicated protection for the female germline". Nature Reviews Molecular Cell Biology. 8 (1): 4–5. doi:10.1038/nrm2091.
  7. ↑ Crum CP, McKeon FD (2010). "p63 in epithelial survival, germ cell surveillance, and neoplasia". Annual Review of Pathology. 5: 349–71. doi:10.1146/annurev-pathol-121808-102117. PMID 20078223.
  8. ↑ Deutsch GB, Zielonka EM, Coutandin D, Weber TA, Schäfer B, Hannewald J, Luh LM, Durst FG, Ibrahim M, Hoffmann J, Niesen FH, Sentürk A, Kunkel H, Brutschy B, Schleiff E, Knapp S, Acker-Palmer A, Grez M, McKeon F, Dötsch V (Feb 2011). "DNA damage in oocytes induces a switch of the quality control factor TAp63α from dimer to tetramer". Cell. 144 (4): 566–76. doi:10.1016/j.cell.2011.01.013. PMC 3087504. PMID 21335238.
  9. ↑ Rouleau M, Medawar A, Hamon L, Shivtiel S, Wolchinsky Z, Zhou H, De Rosa L, Candi E, de la Forest Divonne S, Mikkola ML, van Bokhoven H, Missero C, Melino G, Pucéat M, Aberdam D (Nov 2011). "TAp63 is important for cardiac differentiation of embryonic stem cells and heart development". Stem Cells. 29 (11): 1672–83. doi:10.1002/stem.723. PMID 21898690. Archived from the original on 2014-08-08.
  10. ↑ Su X, Paris M, Gi YJ, Tsai KY, Cho MS, Lin YL, Biernaskie JA, Sinha S, Prives C, Pevny LH, Miller FD, Flores ER (Jul 2009). "TAp63 prevents premature aging by promoting adult stem cell maintenance". Cell Stem Cell. 5 (1): 64–75. doi:10.1016/j.stem.2009.04.003. PMC 3418222. PMID 19570515.
  11. ↑ 11.0 11.1 11.2 11.3 11.4 Dixon MJ, Marazita ML, Beaty TH, Murray JC (Mar 2011). "Cleft lip and palate: understanding genetic and environmental influences". Nature Reviews Genetics. 12 (3): 167–78. doi:10.1038/nrg2933. PMC 3086810. PMID 21331089.
  12. ↑ Shalom-Feuerstein R, Serror L, Aberdam E, Müller FJ, van Bokhoven H, Wiman KG, et al. (February 2013). "Impaired epithelial differentiation of induced pluripotent stem cells from ectodermal dysplasia-related patients is rescued by the small compound APR-246/PRIMA-1MET". Proceedings of the National Academy of Sciences of the United States of America. 110 (6): 2152–6. doi:10.1073/pnas.1201753109. PMC 3568301. PMID 23355677.
  13. ↑ Shiran MS, Tan GC, Sabariah AR, Rampal L, Phang KS (Mar 2007). "p63 as a complimentary basal cell specific marker to high molecular weight-cytokeratin in distinguishing prostatic carcinoma from benign prostatic lesions". The Medical Journal of Malaysia. 62 (1): 36–9. PMID 17682568.
  14. ↑ Herawi M, Epstein JI (Jun 2007). "Immunohistochemical antibody cocktail staining (p63/HMWCK/AMACR) of ductal adenocarcinoma and Gleason pattern 4 cribriform and noncribriform acinar adenocarcinomas of the prostate". The American Journal of Surgical Pathology. 31 (6): 889–94. doi:10.1097/01.pas.0000213447.16526.7f. PMID 17527076.
  15. ↑ Zhang H, Liu J, Cagle PT, Allen TC, Laga AC, Zander DS (Jan 2005). "Distinction of pulmonary small cell carcinoma from poorly differentiated squamous cell carcinoma: an immunohistochemical approach". Modern Pathology. 18 (1): 111–8. doi:10.1038/modpathol.3800251. PMID 15309021.
  16. ↑ Fomenkov A, Huang YP, Topaloglu O, Brechman A, Osada M, Fomenkova T, Yuriditsky E, Trink B, Sidransky D, Ratovitski E (Jun 2003). "P63 alpha mutations lead to aberrant splicing of keratinocyte growth factor receptor in the Hay-Wells syndrome". The Journal of Biological Chemistry. 278 (26): 23906–14. doi:10.1074/jbc.M300746200. PMID 12692135.
  17. ↑ Yi R, Poy MN, Stoffel M, Fuchs E (Mar 2008). "A skin microRNA promotes differentiation by repressing 'stemness'". Nature. 452 (7184): 225–9. doi:10.1038/nature06642. PMC 4346711. PMID 18311128.
  18. ↑ Aberdam D, Candi E, Knight RA, Melino G (Dec 2008). "miRNAs, 'stemness' and skin". Trends in Biochemical Sciences. 33 (12): 583–91. doi:10.1016/j.tibs.2008.09.002. PMID 18848452. Archived from the original on 2013-04-21.

Further reading

External links

Retrieved from "https://www.wikidoc.org/index.php?title=TP63&oldid=1541747"