Ask about this productRelated genes to: MITF antibody
- Gene:
- MITF NIH gene
- Name:
- melanocyte inducing transcription factor
- Previous symbol:
- WS2A, WS2
- Synonyms:
- MI, bHLHe32
- Chromosome:
- 3p13
- Locus Type:
- gene with protein product
- Date approved:
- 1993-10-27
- Date modifiied:
- 2019-04-23
Related products to: MITF antibody
Related articles to: MITF antibody
- Ground-level ozone, a major air pollutant, primarily forms through photochemical reactions between nitrogen oxides (NOx) and volatile organic compounds (VOCs) in sunlight. Ozone is known to harm human health and skin, making it a significant environmental concern. In this study, we examined the effects of ozone exposure on melanogenesis and whether resveratrol could influence this process. Using zebrafish models and B16F10 melanoma cells, we assessed changes in melanin production. In B16F10 cells, we investigated the impact of 1 ppm ozone exposure on reactive oxygen species (ROS) production and its subsequent effect on mitogen-activated protein kinase (MAPK) signaling pathways, including the extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38. Our findings showed that ozone exposure significantly increased melanin levels in both zebrafish and B16F10 cells. Ozone exposure enhanced p38 and JNK phosphorylation, reduced ERK phosphorylation, and upregulated microphthalmia-associated transcription factor (MITF) and tyrosinase expression. Resveratrol was selected as a candidate agent for its ability to inhibit MAPK signaling. Resveratrol treatment effectively reduced ozone-induced melanin production by decreasing MITF and its downstream enzyme, tyrosinase. These results highlight the role of MAPK signaling in ozone-induced pigmentation and suggest that resveratrol could be a promising agent for protecting against ozone-related skin damage. - Source: PubMed
Publication date: 2026/07/15
Lee Che-HsinChang Chi-JieLiu Wang-TaChen Pei-HsuanWang Chia C - UV radiation (UVR) drives high mutational burdens, yet precursor melanocytes accumulate these mutations without triggering immune clearance. Here, we investigated whether melanocyte-intrinsic transcriptional program(s) underlie immune tolerance to mutations resulting from UVR exposure. In primary human melanocytes, expression of PD-L1 (CD274) was dependent on microphthalmia-associated transcription factor (MITF), a crucial regulator of melanocyte development and an intermediate in the UV-tanning pathway. MITF directly activated PD-L1 transcription by binding a conserved upstream enhancer containing functional E-box elements. MITF determined both baseline melanocytic PD-L1 expression in healthy skin and its induction following UVR, independent of interferon signaling. Melanocyte-restricted Pd-l1 deletion in mice triggered CD8 T cell infiltration and depigmentation after long-term UVB exposure, recapitulating features of human vitiligo. PD-L1-deficient human induced pluripotent stem cell (iPSC)-derived melanocytes underwent increased apoptosis and were more susceptible than PD-L1-intact melanocytes to gp100-specific CD8 T cell killing. Thus, a melanocyte-intrinsic MITF-PD-L1 tolerance program protects melanocytes from autoimmune destruction, potentially facilitating early immune evasion during melanoma development and conversely underlying the responsiveness of melanoma to PD-1/PD-L1 blockade. - Source: PubMed
Publication date: 2026/08/13
Lo Jennifer ARachmin InbalFlesher Jessica LWu XunweiKawakami AkinoriHejna MiroslavBoozer Judith RNguyen NhuKing Andrew DJi YawenGermana SharonKemeny Lajos Vvan der Sande Anita A JCheng Jeffrey BLotem MichalUtne Torrey RZhan YaoRoider Elisabeth MMujahid NismaByrne Elizabeth HSingh ShailbalaSaidani ManoubiaMartineau SabrinaHolic NathalieBaldeschi ChristineMartinat CécileFreeman Gordon JHacohen NirFlaherty Keith TBoland Genevieve MSong Jun SSharpe Arlene HDemehri ShadmehrYee CassianAllouche JenniferFisher David E - Molecular advances have expanded the spectrum of cutaneous soft tissue tumours, leading to the recognition of several recently described entities with distinct genetic drivers. This review outlines the defining histopathological, immunophenotypic and molecular features of hybrid superficial ALK-rearranged myxoid spindle cell neoplasm/epithelioid fibrous histiocytoma, superficial neurocristic tumour, ALK-rearranged epithelioid vascular neoplasm and MITF pathway-activated melanocytic tumour. Key diagnostic features and differential considerations are highlighted, with attention to areas of morphological overlap and current gaps in biological characterization. This synthesis aims to facilitate accurate recognition and classification of these emerging tumours in routine dermatopathology practice. - Source: PubMed
Publication date: 2026/08/13
Shafi SabaDermawan Josephine K - Conventional tyrosinase (TYR) inhibitors irritate skin and trigger rebound pigmentation, necessitating safer and more effective depigmenting agents. - Source: PubMed
Publication date: 2026/08/04
Wang JingtingQian YuerongGong QingnaHe RuiTian ShanliYu NannanXi YananWu QiqiWang Guang-LiWang Jing - Valorizing agricultural byproducts into functional ingredients is highly desirable. Herein, plant-derived nanovesicles (PDNVs) from stems/leaves (SL-EXO) exhibited potent anti-melanogenic properties, whereas root-derived PDNVs were ineffective. In vitro, SL-EXO achieved 92.66% cell-free tyrosinase inhibition, while α-arbutin was 49.78%. In vivo, SL-EXO ameliorated the pigmentation-driving oxidative/senescent microenvironment in zebrafish and reduced macroscopic melanin by ~66%. Crucially, SL-EXO reversed α-MSH-induced hyperpigmentation in B16F10 cells while maintaining excellent biocompatibility up to 0.15 mg/mL, displaying a vastly superior safety margin compared to α-arbutin (which induced cytotoxicity at 0.075 mg/mL). To decode this, multi-omics profiling revealed that SL-EXO utilizes a chloroplast-derived biomimetic lipid architecture (enriched in MGDG/DGDG) to efficiently deliver potent flavonoid payloads. Molecular docking demonstrated exceptional predictive structural affinities (binding energies up to -10.9 kcal/mol) between these phytochemicals and AKT1. Finally, pharmacological rescue assays validated that SL-EXO arrests melanogenesis by targeting the AKT1 pathway, thereby downregulating the p-AKT/p-GSK3/MITF signaling cascade and silencing melanogenic genes. This study establishes a rigorous multi-omics paradigm for upcycling botanical wastes into exceptionally safe and efficacious natural anti-melanogenic nanotherapeutics. - Source: PubMed
Publication date: 2026/08/05
Feng PeishiTao LiChen XiaoliYang HanZhang YidaWang Ping