ArticleGenes & development2005
The cleavage of microphthalmia-associated transcription factor, MITF, by caspases plays an essential role in melanocyte and melanoma cell apoptosis.
Article in Genes & development, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 65 citations in OpenAlex.
- MITF Regulates CFTR Expression to Participate in Myocardial Ischemia-Reperfusion Injury.The journal of gene medicine · 2026Article
- Novel mechanisms of MITF regulation identified in a mouse suppressor screen.EMBO reports · 2024Article
- Transcriptional variations at perilesional site in vitiligo patients: probably a fight for cell-survival.Archives of dermatological research · 2024Article
- Mitf regulates gene expression networks implicated in B cell homeostasis, germinal center responses, and tolerance.Frontiers in immunology · 2024Article
- Novel mechanisms of MITF regulation and melanoma predisposition identified in a mouse suppressor screen.bioRxiv : the preprint server for biology · 2023Article
- The underestimated role of the microphthalmia-associated transcription factor (MiTF) in normal and pathological haematopoiesis.Cell & bioscience · 2021Review
- MITF-the first 25 years.Genes & development · 2019Review
- Lysosomal acid ceramidase ASAH1 controls the transition between invasive and proliferative phenotype in melanoma cells.Oncogene · 2019Article
- Microphthalmia-Associated Transcription Factor (MITF) Regulates Immune Cell Migration into Melanoma.Translational oncology · 2019Article
- Cycloartane triterpenoid (23R, 24E)-23-acetoxymangiferonic acid inhibited proliferation and migration in B16-F10 melanoma via MITF downregulation caused by inhibition of both β-catenin and c-Raf-MEK1-ERK signaling axis.Journal of natural medicines · 2019Article
- A direct link between MITF, innate immunity, and hair graying.PLoS biology · 2018Article
- Parthenolide induces MITF-M downregulation and senescence in patient-derived MITF-M(high) melanoma cell populations.Oncotarget · 2016Article
- MITF in melanoma: mechanisms behind its expression and activity.Cellular and molecular life sciences : CMLS · 2015Review
- Pro-survival role of MITF in melanoma.The Journal of investigative dermatology · 2015Review
- SIRT1 promotes proliferation and inhibits the senescence-like phenotype in human melanoma cells.Oncotarget · 2014Article
- The MAPK pathway functions as a redundant survival signal that reinforces the PI3K cascade in c-Kit mutant melanoma.Oncogene · 2014Article
- Secretome from senescent melanoma engages the STAT3 pathway to favor reprogramming of naive melanoma towards a tumor-initiating cell phenotype.Oncotarget · 2013Article
- A myosin-Va tail fragment sequesters dynein light chains leading to apoptosis in melanoma cells.Cell death & disease · 2013Article
- Article
- Aurora B is regulated by the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling pathway and is a valuable potential target in melanoma cells.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microphthalmia-associated transcription factor (MITF) M-form is a melanocyte-specific transcription factor that plays a key role in melanocyte development, survival, and differentiation. Here, we identified MITF as a new substrate of caspases and we characterized the cleavage site after Asp 345 in the C-terminal domain. We show that expression of a noncleavable form of MITF renders melanoma cells resistant to apoptotic stimuli, and we found that the C-terminal fragment generated upon caspase cleavage is endowed with a proapoptotic activity that sensitizes melanoma cells to death signals. The proapoptotic function gained by MITF following its processing by caspases provides a tissue-restricted means to modulate death in melanocyte and melanoma cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.