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Article: Phosphorylation of MITF by AKT affects its downstream targets and causes TP53-dependent cell senescence
Title | Phosphorylation of MITF by AKT affects its downstream targets and causes TP53-dependent cell senescence |
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Authors | |
Keywords | AKT MITF Phosphorylation Senescence TP53 |
Issue Date | 2016 |
Publisher | Elsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/biocel |
Citation | The International Journal of Biochemistry & Cell Biology, 2016, v. 80, p. 132-142 How to Cite? |
Abstract | Microphthalmia-associated transcription factor (MITF) plays a crucial role in the melanogenesis and proliferation of melanocytes that is dependent on its abundance and modification. Here, we report that epidermal growth factor (EGF) induces senescence and cyclin-dependent kinase inhibitor 1A (CDKN1A) expression that is related to MITF. We found that MITF could bind TP53 to regulate CDKN1A. Furthermore, the interaction between MITF and TP53 is dependent on AKT activity. We found that AKT phosphorylates MITF at S510. Phosphorylated MITF S510 enhances its affinity to TP53 and promotes CDKN1A expression. Meanwhile, the unphosphorylative MITF promotes TYR expression. The levels of p-MITF-S510 are low in 90% human melanoma samples. Thus the level of p-MITF-S510 could be a possible diagnostic marker for melanoma. Our findings reveal a mechanism for regulating MITF functions in response to EGF stimulation and suggest a possible implementation for preventing the over proliferation of melanoma cells. |
Persistent Identifier | http://hdl.handle.net/10722/243568 |
ISSN | 2023 Impact Factor: 3.4 2023 SCImago Journal Rankings: 1.079 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Wang, C | - |
dc.contributor.author | Zhao, L | - |
dc.contributor.author | Su, Q | - |
dc.contributor.author | Fan, X | - |
dc.contributor.author | Wang, Y | - |
dc.contributor.author | Gao, S | - |
dc.contributor.author | Wang, H | - |
dc.contributor.author | Chen, H | - |
dc.contributor.author | Chan, CB | - |
dc.contributor.author | Liu, Z | - |
dc.date.accessioned | 2017-08-25T02:56:35Z | - |
dc.date.available | 2017-08-25T02:56:35Z | - |
dc.date.issued | 2016 | - |
dc.identifier.citation | The International Journal of Biochemistry & Cell Biology, 2016, v. 80, p. 132-142 | - |
dc.identifier.issn | 1357-2725 | - |
dc.identifier.uri | http://hdl.handle.net/10722/243568 | - |
dc.description.abstract | Microphthalmia-associated transcription factor (MITF) plays a crucial role in the melanogenesis and proliferation of melanocytes that is dependent on its abundance and modification. Here, we report that epidermal growth factor (EGF) induces senescence and cyclin-dependent kinase inhibitor 1A (CDKN1A) expression that is related to MITF. We found that MITF could bind TP53 to regulate CDKN1A. Furthermore, the interaction between MITF and TP53 is dependent on AKT activity. We found that AKT phosphorylates MITF at S510. Phosphorylated MITF S510 enhances its affinity to TP53 and promotes CDKN1A expression. Meanwhile, the unphosphorylative MITF promotes TYR expression. The levels of p-MITF-S510 are low in 90% human melanoma samples. Thus the level of p-MITF-S510 could be a possible diagnostic marker for melanoma. Our findings reveal a mechanism for regulating MITF functions in response to EGF stimulation and suggest a possible implementation for preventing the over proliferation of melanoma cells. | - |
dc.language | eng | - |
dc.publisher | Elsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/biocel | - |
dc.relation.ispartof | The International Journal of Biochemistry & Cell Biology | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject | AKT | - |
dc.subject | MITF | - |
dc.subject | Phosphorylation | - |
dc.subject | Senescence | - |
dc.subject | TP53 | - |
dc.title | Phosphorylation of MITF by AKT affects its downstream targets and causes TP53-dependent cell senescence | - |
dc.type | Article | - |
dc.identifier.email | Chan, CB: chancb@hku.hk | - |
dc.identifier.authority | Chan, CB=rp02140 | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1016/j.biocel.2016.09.029 | - |
dc.identifier.scopus | eid_2-s2.0-84991713047 | - |
dc.identifier.hkuros | 274300 | - |
dc.identifier.volume | 80 | - |
dc.identifier.spage | 132 | - |
dc.identifier.epage | 142 | - |
dc.identifier.isi | WOS:000388053400015 | - |
dc.publisher.place | United Kingdom | - |
dc.identifier.issnl | 1357-2725 | - |