MITF (microphthalmia-associated transcription factor)
2013-04-01 Nicole D Riddle , Paul Zhang AffiliationDepartment of Pathology, University of Texas Health Science Center, San Antonio, TX, USA (NDR); Department of Pathology, University of Pennsylvania Health System, Philadelphia, PA, USA (PZ)
Identity
HGNC
LOCATION
3p14.1
IMAGE
LOCUSID
ALIAS
CMM8,COMMAD,MI,WS2,WS2A,bHLHe32
FUSION GENES
DNA/RNA
Description
The gene encompasses 229 kb, and has 9 exons.
Transcription
Nine different isoforms have been described for MITF, each with different 5 specificity (MITF -A, -J, -C, -MC, -E, -H, -D, -B, -M). All isoforms have exons 2-9 in common, encoding the functional domains of the transcription factors. Exon 1 is variable and the domains within it are the transactivation domain (TAD) and the beta-helix-loop-helix-zipper (B-HLH-Zip). Some isoforms are specific for certain cells types, i.e. M: melanocytes, MC: mast cells (Levy et al., 2006).
Proteins
Description
526 aa, 58795 Da.
Regulates the differentiation and development of melanocytes, neural crest-derived cells, retinal epithelium (optic cup-derived retinal pigment epithelium), mast cells, and osteoclasts (Lin and Fisher, 2007; Adijanto et al., 2012).
Regulates the differentiation and development of melanocytes, neural crest-derived cells, retinal epithelium (optic cup-derived retinal pigment epithelium), mast cells, and osteoclasts (Lin and Fisher, 2007; Adijanto et al., 2012).
Post translational modifications:
- Phosphorylation at Ser-405 significantly enhances the ability to bind the tyrosinase promoter.
- Phosphorylation at Ser-180 and Ser-516 by MAPK and RPS6KA1 activate the transcription factor activity and promote ubiquitiniation and subsequent degradation.
- Can be deubiquitinated by USP13, preventing its degradation.
Expression
Found in most human tissues. Particularly high quantities in retina, uterus, pineal gland, and adipocytes (biogps.org).
Localisation
Nucleus.
Function
A transcription factor that activates the transcription of tyrosinase and tyrosinase-related protein 1 (TYRP1), and dopachrome tautomerase (DCT). These are enzymes that are specifically expressed in melanocytes (Yasumoto et al., 1995). For tyrosinase, MITF binds to a symmetrical DNA sequence found in the promoter region: a restricted subset of E-box motives containing canonical CATGTG sequence flanked by a 5 thymidine (Aksan and Goding, 1998). The regulation of the DCT promoter is even more complex and involves other proteins like CREB and SOX10; and PAX3 has an inhibitory effect on DCT activation by MITF (Bertolotto et al., 1998; Ludwig et al., 2004; Lang et al., 2005).
Not only does MITF activate genes involved in melanin synthesis, it also activates the transcription of genes involved in melanosome structure (PMEL17, MART-1), biogenesis (ocular albinism type 1 gene), and transport (RAB27A) (Du et al., 2003; Vetrini et al., 2004; Chiaverini et al., 2008). Also, MITF activates the transcription of the melanocortin 1 receptor gene which encodes a melanocyte-stimulating hormone receptor normally present on the plasma membrane of melanocytes: this binding is the first step in the hormonal regulation of pigmentation (Vachtenheim and Borovansky, 2010).
In addition, MITF plays a role in apoptosis through several target genes, showing importance of MITF in melanocyte development and survival. MITF controls the transcription of BCL-2, and known inhibitor of apoptosis (McGill et al., 2002). Therefore, MITF mutation may explain the reduced number of melanocytes in certain disorders (Samija et al., 2010). MITF also induces transcription of melanoma-inhibitor-of-apoptosis (BIRC7, ML-IAP) (Dynek et al., 2008). Furthermore, it regulates a receptor for hepatocyte growth factor (MET), whose activation inhibits melanocyte apoptosis (Beuret et al., 2007).
MITF also plays a role in melanocyte proliferation by regulating several genes involved in the cell-cycle: cyclin-dependant kinase 2 (CDK2), transcription factor TBX2, and Dia1 protein (Diaph1). These promote cell-cycle progression, prevent senescence and cell-cycle arrest, and increase cellular proliferation, respectively (Du et al., 2004; Carreira et al., 2005; Carreira et al., 2006). However, MITF also has anti-proliferative properties by way of inducing cell-cycle arrest by activating cyclin-dependent kinase inhibitor 1A and 2A (CDKN1A/p21, CDKN2A/p16) (Carreira et al., 2005; Loercher et al., 2005). It has believed that both depletion and over-expression inhibit proliferation whereas normal levels promote proliferation (Kido et al., 2009).
MITF also has important roles in osteoclast and mast cell development and function. In osteoclasts it activates transcription of functional proteins tartrate-resistant alkaline phosphatase (TRAP), cathepsin K, OSCAR, e-cadherin, OSTM1 and CLCN7 (Meadows et al., 2007). In mast cells MITF activates the transcription of mast cell proteases 2,4,5,6, and 9, granzyme B, tryptophan hydroxylase, and kit, all important for differentiation and function (Kitamura et al., 2006).
Up-stream regulation: LysRS-Ap4A-MITF signaling pathway (Lee et al., 2004); Wnt signaling pathway (Takeda et al., 2000); alpha melanocyte-stimulating hormone signaling pathway (Bertolotto et al., 1998).
Not only does MITF activate genes involved in melanin synthesis, it also activates the transcription of genes involved in melanosome structure (PMEL17, MART-1), biogenesis (ocular albinism type 1 gene), and transport (RAB27A) (Du et al., 2003; Vetrini et al., 2004; Chiaverini et al., 2008). Also, MITF activates the transcription of the melanocortin 1 receptor gene which encodes a melanocyte-stimulating hormone receptor normally present on the plasma membrane of melanocytes: this binding is the first step in the hormonal regulation of pigmentation (Vachtenheim and Borovansky, 2010).
In addition, MITF plays a role in apoptosis through several target genes, showing importance of MITF in melanocyte development and survival. MITF controls the transcription of BCL-2, and known inhibitor of apoptosis (McGill et al., 2002). Therefore, MITF mutation may explain the reduced number of melanocytes in certain disorders (Samija et al., 2010). MITF also induces transcription of melanoma-inhibitor-of-apoptosis (BIRC7, ML-IAP) (Dynek et al., 2008). Furthermore, it regulates a receptor for hepatocyte growth factor (MET), whose activation inhibits melanocyte apoptosis (Beuret et al., 2007).
MITF also plays a role in melanocyte proliferation by regulating several genes involved in the cell-cycle: cyclin-dependant kinase 2 (CDK2), transcription factor TBX2, and Dia1 protein (Diaph1). These promote cell-cycle progression, prevent senescence and cell-cycle arrest, and increase cellular proliferation, respectively (Du et al., 2004; Carreira et al., 2005; Carreira et al., 2006). However, MITF also has anti-proliferative properties by way of inducing cell-cycle arrest by activating cyclin-dependent kinase inhibitor 1A and 2A (CDKN1A/p21, CDKN2A/p16) (Carreira et al., 2005; Loercher et al., 2005). It has believed that both depletion and over-expression inhibit proliferation whereas normal levels promote proliferation (Kido et al., 2009).
MITF also has important roles in osteoclast and mast cell development and function. In osteoclasts it activates transcription of functional proteins tartrate-resistant alkaline phosphatase (TRAP), cathepsin K, OSCAR, e-cadherin, OSTM1 and CLCN7 (Meadows et al., 2007). In mast cells MITF activates the transcription of mast cell proteases 2,4,5,6, and 9, granzyme B, tryptophan hydroxylase, and kit, all important for differentiation and function (Kitamura et al., 2006).
Up-stream regulation: LysRS-Ap4A-MITF signaling pathway (Lee et al., 2004); Wnt signaling pathway (Takeda et al., 2000); alpha melanocyte-stimulating hormone signaling pathway (Bertolotto et al., 1998).
Mutations
Note
The MITF promoter is partially regulated by certain transcription factors such as PAX3, SOX10, LEF-1/TCF and CREB during development. Mutations affecting the MITF and the MITF pathway lead to pigmentary and auditory defects (Cimadamore et al., 2012; Pierrat et al., 2012).
Germinal
Mutations in the MITF at germline will lead to syndromes with pigmentary and/or auditory defects. Mutations in MITF are also known to give a predisposition to certain cancers, including melanoma and renal cell carcinoma (Bertolotto et al., 2011). Heterozygous mutations lead to auditory/pigmentary syndromes such as Waardenburg type 2 and Tietz syndrome (Lin and Fisher, 2007).
Implicated in
Entity name
Melanoma
Note
A malignant neoplasm of melanocytes, arising either from pre-existing benign nevi or de novo and occurring most commonly on the skin, but may occur in other locations.
In addition, BRAF mutations (found in ~60% of melanomas) have a two-fold regulation of MITF transcription and is believed to keep MITF at appropriate levels promoting melanoma cell proliferation and survival. Supporting this theory is the fact that pure up-regulation of MITF inhibits melanoma cell proliferation and re-expression reduces tumorigenecity in vivo (Wellbrock and Marais, 2005). And MITF expression by immunohistochemistry has been shown to decrease with disease progression, and be a predictor of overall and disease-free survival (Salti et al., 2000; Zhuang et al., 2007).
MITF amplification has also been associated with decreased survival and chemoresistance (Gallaway et al., 2005). It is postulated the MITF may be a lineage specific oncogene in melanoma, particularly in the subset with CDKN2A mutations (Garraway and Sellers, 2006; Bennett, 2008). This hypothesis is supported by research that has shown that all melanoma cell lines that had MITF gene amplifications also had CDKN2A pathway inactivation (Gallaway et al., 2005). MITFs role as a lineage specific oncogene is also supported by its important part in cell growth, survival, growth, and proliferation through BCL2, CDK2, TBX2, ML-IAP etc, as described above.
As mentioned above, MITF is not expressed in all melanomas. This indicates that there are different subsets of melanomas which differ in their need of MITF for their progression and survival (Salti et al., 2000; Miettinen et al., 2001; Granter et al., 2002). There is also evidences that the role of MITF may change within a melanoma during progression (Hoek et al., 2008a).
In addition, BRAF mutations (found in ~60% of melanomas) have a two-fold regulation of MITF transcription and is believed to keep MITF at appropriate levels promoting melanoma cell proliferation and survival. Supporting this theory is the fact that pure up-regulation of MITF inhibits melanoma cell proliferation and re-expression reduces tumorigenecity in vivo (Wellbrock and Marais, 2005). And MITF expression by immunohistochemistry has been shown to decrease with disease progression, and be a predictor of overall and disease-free survival (Salti et al., 2000; Zhuang et al., 2007).
MITF amplification has also been associated with decreased survival and chemoresistance (Gallaway et al., 2005). It is postulated the MITF may be a lineage specific oncogene in melanoma, particularly in the subset with CDKN2A mutations (Garraway and Sellers, 2006; Bennett, 2008). This hypothesis is supported by research that has shown that all melanoma cell lines that had MITF gene amplifications also had CDKN2A pathway inactivation (Gallaway et al., 2005). MITFs role as a lineage specific oncogene is also supported by its important part in cell growth, survival, growth, and proliferation through BCL2, CDK2, TBX2, ML-IAP etc, as described above.
As mentioned above, MITF is not expressed in all melanomas. This indicates that there are different subsets of melanomas which differ in their need of MITF for their progression and survival (Salti et al., 2000; Miettinen et al., 2001; Granter et al., 2002). There is also evidences that the role of MITF may change within a melanoma during progression (Hoek et al., 2008a).
Entity name
Renal cell carcinoma
Note
Malignant transformation of the renal parenchyma. Associated with Von Hippel-Lindau syndrome: a rare, autosomal dominant disease predisposing to clear cell renal cell carcinoma, as well as hemangioblastomas, pheochromocytomas, pancreatic cysts and neuroendocrine tumors, endolymphatic sac tumors, and a general increase risk in cancer; results from mutation of the VHL tumor suppressor gene on chromosome 3p.
A subset of renal cell carcinomas, more common in children, are associated with TFE3 mutations, a member of the microphthalmia (MIT) family, closely related to MITF.
Recent studies have shown that the same MITF mutation associated with increased risk of melanoma (E318K) also leads to increased risk of renal cell carcinoma (Bertolotto et al., 2011). However, it is unclear at this time the role that MITF in particular plays in renal tumors. It may be that this mutation leads to disrupted interaction with TFE3. Or it is possible that mechanisms are similar to that of melanoma, however, MITF is not associated with normal kidney function in the same way that it is in normal melanocyte function. Research is ongoing in this area.
A subset of renal cell carcinomas, more common in children, are associated with TFE3 mutations, a member of the microphthalmia (MIT) family, closely related to MITF.
Recent studies have shown that the same MITF mutation associated with increased risk of melanoma (E318K) also leads to increased risk of renal cell carcinoma (Bertolotto et al., 2011). However, it is unclear at this time the role that MITF in particular plays in renal tumors. It may be that this mutation leads to disrupted interaction with TFE3. Or it is possible that mechanisms are similar to that of melanoma, however, MITF is not associated with normal kidney function in the same way that it is in normal melanocyte function. Research is ongoing in this area.
Entity name
Note
A group of autosomal dominant inherited conditions that involve deafness and lack of pigment of the hair, skin, and/or eyes. There are 4 main types of WS, 1 and 2 being most common. MITF is the gene associated with Waardenburg syndrome 2a (WS2a), characterized by sensorineural hearing loss and patches of depigmentation, with or without ocular albinism. These features may show variable expression and penetrance.
Some of the mutations are single or multiple amino acid changes that alter the helix-loop-helix or leucine zipper motif. There are other mutations that create a shortened, non-functional version of MITF. It is believed that all of these mutations disrupt the formation of the dimers necessary for proper function and development; thereby there is an insufficient concentration of the MITF protein within the cytoplasm for normal function (haploinsufficiency). Also, as described above, MITF regulates BCL-2, ML-IAP, and MET. Without adequate amounts of MITF there is over-apoptosis of melanocytes. This leads to a decreased number of melanocytes in certain areas of the skin, hair, eyes, inner ear, etc (Tachibana, 1997; Samija et al., 2010).
Patients with WS1 will have the addition of craniofacial deformities and those with WS3 (Klein-Waardenburg syndrome) have limb deformities, both are due to mutations in PAX3, which is part of the MITF pathway, Those with WS4 (Waardenburg-Shah Syndrome) will also have Hirchsprungs syndrome, associated with mutations in 3 genes: SOX10, endothelin 3, and endothelin receptor B (Tassabehji et al., 1995; Widlund and Fisher, 2003).
Some of the mutations are single or multiple amino acid changes that alter the helix-loop-helix or leucine zipper motif. There are other mutations that create a shortened, non-functional version of MITF. It is believed that all of these mutations disrupt the formation of the dimers necessary for proper function and development; thereby there is an insufficient concentration of the MITF protein within the cytoplasm for normal function (haploinsufficiency). Also, as described above, MITF regulates BCL-2, ML-IAP, and MET. Without adequate amounts of MITF there is over-apoptosis of melanocytes. This leads to a decreased number of melanocytes in certain areas of the skin, hair, eyes, inner ear, etc (Tachibana, 1997; Samija et al., 2010).
Patients with WS1 will have the addition of craniofacial deformities and those with WS3 (Klein-Waardenburg syndrome) have limb deformities, both are due to mutations in PAX3, which is part of the MITF pathway, Those with WS4 (Waardenburg-Shah Syndrome) will also have Hirchsprungs syndrome, associated with mutations in 3 genes: SOX10, endothelin 3, and endothelin receptor B (Tassabehji et al., 1995; Widlund and Fisher, 2003).
Entity name
Tietz syndrome
Note
An autosomal dominant disorder characterized by generalized hypopigmentation (fair skin and light-colored hair) and profound bilateral congenital hearing loss. Penetrance is complete.
The mutation is a change or deletion of a single amino acid in the basic motif region. This resultant altered protein cannot bind to DNA, thereby affecting the development of melanocytes, and therefore, melanin production (Smith et al., 2000). The mechanism is similar to Waardenburg syndrome, but more severe. In a heterozygote the abnormal protein cannot dimerise effectively even with a normal allele product, i.e. even the normal allele does not function. This concept is referred to as a dominant negative. There is effectively no normal MITF available (Smith et al., 2000).
The mutation is a change or deletion of a single amino acid in the basic motif region. This resultant altered protein cannot bind to DNA, thereby affecting the development of melanocytes, and therefore, melanin production (Smith et al., 2000). The mechanism is similar to Waardenburg syndrome, but more severe. In a heterozygote the abnormal protein cannot dimerise effectively even with a normal allele product, i.e. even the normal allele does not function. This concept is referred to as a dominant negative. There is effectively no normal MITF available (Smith et al., 2000).
Article Bibliography
| Pubmed ID | Last Year | Title | Authors |
|---|---|---|---|
| 22523078 | 2012 | Microphthalmia-associated transcription factor (MITF) promotes differentiation of human retinal pigment epithelium (RPE) by regulating microRNAs-204/211 expression. | Adijanto J et al |
| 9819381 | 1998 | Targeting the microphthalmia basic helix-loop-helix-leucine zipper transcription factor to a subset of E-box elements in vitro and in vivo. | Aksan I et al |
| 18353141 | 2008 | How to make a melanoma: what do we know of the primary clonal events? | Bennett DC et al |
| 22012259 | 2011 | A SUMOylation-defective MITF germline mutation predisposes to melanoma and renal carcinoma. | Bertolotto C et al |
| 17371876 | 2007 | Up-regulation of MET expression by alpha-melanocyte-stimulating hormone and MITF allows hepatocyte growth factor to protect melanocytes and melanoma cells from apoptosis. | Beuret L et al |
| 19578364 | 2009 | Genome-wide association study identifies three loci associated with melanoma risk. | Bishop DT et al |
| 17182868 | 2006 | Mitf regulation of Dia1 controls melanoma proliferation and invasiveness. | Carreira S et al |
| 18281284 | 2008 | Microphthalmia-associated transcription factor regulates RAB27A gene expression and controls melanosome transport. | Chiaverini C et al |
| 22571403 | 2012 | SOX2 modulates levels of MITF in normal human melanocytes, and melanoma lines in vitro. | Cimadamore F et al |
| 19422606 | 2009 | Frequent mutations in the MITF pathway in melanoma. | Cronin JC et al |
| 20164056 | 2011 | TFE3 expression in tumors of the microphthalmia-associated transcription factor (MiTF) family. | Dickson BC et al |
| 12819038 | 2003 | MLANA/MART1 and SILV/PMEL17/GP100 are transcriptionally regulated by MITF in melanocytes and melanoma. | Du J et al |
| 15607961 | 2004 | Critical role of CDK2 for melanoma growth linked to its melanocyte-specific transcriptional regulation by MITF. | Du J et al |
| 18451137 | 2008 | Microphthalmia-associated transcription factor is a critical transcriptional regulator of melanoma inhibitor of apoptosis in melanomas. | Dynek JN et al |
| 16862190 | 2006 | Lineage dependency and lineage-survival oncogenes in human cancer. | Garraway LA et al |
| 22647378 | 2012 | The tumor suppressor HINT1 regulates MITF and β-catenin transcriptional activity in melanoma cells. | Genovese G et al |
| 12844286 | 2003 | Localization of a novel melanoma susceptibility locus to 1p22. | Gillanders E et al |
| 11893035 | 2002 | Role for microphthalmia transcription factor in the diagnosis of metastatic malignant melanoma. | Granter SR et al |
| 18245463 | 2008 | In vivo switching of human melanoma cells between proliferative and invasive states. | Hoek KS et al |
| 19067971 | 2008 | Novel MITF targets identified using a two-step DNA microarray strategy. | Hoek KS et al |
| 19659611 | 2009 | Simultaneous suppression of MITF and BRAF V600E enhanced inhibition of melanoma cell proliferation. | Kido K et al |
| 16931285 | 2006 | Molecular mechanisms of mast cell development. | Kitamura Y et al |
| 15729346 | 2005 | Pax3 functions at a nodal point in melanocyte stem cell differentiation. | Lang D et al |
| 14975237 | 2004 | The function of lysyl-tRNA synthetase and Ap4A as signaling regulators of MITF activity in FcepsilonRI-activated mast cells. | Lee YN et al |
| 16899407 | 2006 | MITF: master regulator of melanocyte development and melanoma oncogene. | Levy C et al |
| 17314970 | 2007 | Melanocyte biology and skin pigmentation. | Lin JY et al |
| 15623583 | 2005 | MITF links differentiation with cell cycle arrest in melanocytes by transcriptional activation of INK4A. | Loercher AE et al |
| 14706856 | 2004 | Melanocyte-specific expression of dopachrome tautomerase is dependent on synergistic gene activation by the Sox10 and Mitf transcription factors. | Ludwig A et al |
| 12086670 | 2002 | Bcl2 regulation by the melanocyte master regulator Mitf modulates lineage survival and melanoma cell viability. | McGill GG et al |
| 17105730 | 2007 | The expression of Clcn7 and Ostm1 in osteoclasts is coregulated by microphthalmia transcription factor. | Meadows NA et al |
| 11176069 | 2001 | Microphthalmia transcription factor in the immunohistochemical diagnosis of metastatic melanoma: comparison with four other melanoma markers. | Miettinen M et al |
| 22496449 | 2012 | Expression of microphthalmia-associated transcription factor (MITF), which is critical for melanoma progression, is inhibited by both transcription factor GLI2 and transforming growth factor-β. | Pierrat MJ et al |
| 11016620 | 2000 | Micropthalmia transcription factor: a new prognostic marker in intermediate-thickness cutaneous malignant melanoma. | Salti GI et al |
| 10851256 | 2000 | Tietz syndrome (hypopigmentation/deafness) caused by mutation of MITF. | Smith SD et al |
| 9170159 | 1997 | Evidence to suggest that expression of MITF induces melanocyte differentiation and haploinsufficiency of MITF causes Waardenburg syndrome type 2A. | Tachibana M et al |
| 10747853 | 2000 | Induction of melanocyte-specific microphthalmia-associated transcription factor by Wnt-3a. | Takeda K et al |
| 8589691 | 1995 | The mutational spectrum in Waardenburg syndrome. | Tassabehji M et al |
| 10760582 | 2000 | Structural organization of the human microphthalmia-associated transcription factor gene containing four alternative promoters. | Udono T et al |
| 20201954 | 2010 | "Transcription physiology" of pigment formation in melanocytes: central role of MITF. | Vachtenheim J et al |
| 15781639 | 2005 | Tbx2 is overexpressed and plays an important role in maintaining proliferation and suppression of senescence in melanomas. | Vance KW et al |
| 15254223 | 2004 | The microphthalmia transcription factor (Mitf) controls expression of the ocular albinism type 1 gene: link between melanin synthesis and melanosome biogenesis. | Vetrini F et al |
| 18287284 | 2008 | Intersubunit linker length as a modifier of protein stability: crystal structures and thermostability of mutant TRAP. | Watanabe M et al |
| 16129781 | 2005 | Elevated expression of MITF counteracts B-RAF-stimulated melanocyte and melanoma cell proliferation. | Wellbrock C et al |
| 12789278 | 2003 | Microphthalamia-associated transcription factor: a critical regulator of pigment cell development and survival. | Widlund HR et al |
| 8749302 | 1995 | Transcriptional activation of the melanocyte-specific genes by the human homolog of the mouse Microphthalmia protein. | Yasumoto K et al |
| 22080950 | 2011 | A novel recurrent mutation in MITF predisposes to familial and sporadic melanoma. | Yokoyama S et al |
| 17384650 | 2007 | Mcl-1, Bcl-XL and Stat3 expression are associated with progression of melanoma whereas Bcl-2, AP-2 and MITF levels decrease during progression of melanoma. | Zhuang L et al |
Other Information
Locus ID:
NCBI: 4286
MIM: 156845
HGNC: 7105
Ensembl: ENSG00000187098
Variants:
dbSNP: 4286
ClinVar: 4286
TCGA: ENSG00000187098
COSMIC: MITF
RNA/Proteins
Expression (GTEx)
Pathways
Protein levels (Protein atlas)
References
| Pubmed ID | Year | Title | Citations |
|---|---|---|---|
| 37559350 | 2024 | Modeling of pigmentation disorders associated with MITF mutation in Waardenburg syndrome revealed an impaired melanogenesis pathway in iPS-derived melanocytes. | 1 |
| 38351314 | 2024 | Emerging roles of MITF as a crucial regulator of immunity. | 1 |
| 38456491 | 2024 | MITF regulates the subcellular location of HIF1α through SUMOylation to promote the invasion and metastasis of daughter cells derived from polyploid giant cancer cells. | 1 |
| 37559350 | 2024 | Modeling of pigmentation disorders associated with MITF mutation in Waardenburg syndrome revealed an impaired melanogenesis pathway in iPS-derived melanocytes. | 1 |
| 38351314 | 2024 | Emerging roles of MITF as a crucial regulator of immunity. | 1 |
| 38456491 | 2024 | MITF regulates the subcellular location of HIF1α through SUMOylation to promote the invasion and metastasis of daughter cells derived from polyploid giant cancer cells. | 1 |
| 36241703 | 2023 | The microphthalmia-associated transcription factor is involved in gastrointestinal stromal tumor growth. | 5 |
| 36627143 | 2023 | Novel role of microphthalmia-associated transcription factor in modulating the differentiation and immunosuppressive functions of myeloid-derived suppressor cells. | 1 |
| 36768146 | 2023 | MiR-182 Is Upregulated in Prostate Cancer and Contributes to Tumor Progression by Targeting MITF. | 5 |
| 36787085 | 2023 | Integrative analyses of RNA-seq and ChIP-seq Reveal MITF as a Target Gene of TFPI-2 in MDA231 Cells. | 0 |
| 36834926 | 2023 | MITF Downregulation Induces Death in Human Mast Cell Leukemia Cells and Impairs IgE-Dependent Degranulation. | 3 |
| 37236596 | 2023 | Ataxia Telangiectasia Mutated Signaling Delays Skin Pigmentation upon UV Exposure by Mediating MITF Function toward DNA Repair Mode. | 2 |
| 37658191 | 2023 | GREB1 isoform 4 is specifically transcribed by MITF and required for melanoma proliferation. | 0 |
| 37770430 | 2023 | Acetylation reprograms MITF target selectivity and residence time. | 2 |
| 36241703 | 2023 | The microphthalmia-associated transcription factor is involved in gastrointestinal stromal tumor growth. | 5 |
Citation
Nicole D Riddle ; Paul Zhang
MITF (microphthalmia-associated transcription factor)
Atlas Genet Cytogenet Oncol Haematol. 2013-04-01
Online version: http://atlasgeneticsoncology.org/gene/44193/new-content/
