MITF ELISA Kit
- Known as:
- MITF Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- EK2100
- Product Quantity:
- kit
- Category:
- Peptides
- Supplier:
- Panomics
- Gene target:
- MITF ELISA Kit
Related genes to: MITF ELISA Kit
- 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
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- Growth differentiation factor 15 (GDF15) is a stress-responsive cytokine that has emerged as a pleiotropic regulator in skin biology, yet its context-dependent functions-ranging from protective to pathogenic-remain incompletely understood. This narrative review systematically synthesizes current evidence on the expression patterns, signaling mechanisms, and disease associations of GDF15 in cutaneous health and disease, with particular emphasis on melanogenesis, skin aging, photoaging, and immune-mediated dermatoses including psoriasis, systemic lupus erythematosus, and systemic sclerosis. We propose a four-parameter framework-inducing stimulus, responding cell type, exposure kinetics, and microenvironmental context-that reconciles the apparently contradictory effects of GDF15 across different skin compartments and disease phases. Mechanistically, GDF15 activates β-catenin/MITF/tyrosinase signaling in melanocytes to drive pigmentation, modulates fibroblast collagen synthesis via SMAD2/3 and SASP-associated pathways, and interfaces with the IL-23/Th17 and NF-κB axes in inflammatory skin diseases. Critically, we identify and discuss unresolved knowledge gaps, including the identity of the peripheral receptor(s) mediating GDF15's cutaneous actions, the distinction between correlation and causation in human disease, and the therapeutic challenges posed by GDF15's dual protective and deleterious roles. By integrating mechanistic insights with clinical observations and providing a critical assessment of current evidence levels, this review establishes GDF15 as a multi-node signaling hub in dermatology while offering a balanced roadmap for future translational research-emphasizing that the primary near-term value of GDF15 lies in biomarker development for disease monitoring and patient stratification, rather than in immediate therapeutic targeting. - Source: PubMed
Publication date: 2026/07/31
Wang RuijunTan HaopengLi ZhiqiLi DongmeiPan YuanmingHe Zhanbiao - Abnormal skin pigmentation is a common clinical dermatological issue, and its occurrence and development are closely associated with the inflammatory microenvironment. However, the interactive regulatory mechanisms between inflammatory factors and melanogenesis remain incompletely understood. In this study, through the analysis of transcriptomic data from melasma, psoriasis, acne, atopic dermatitis, and ultraviolet-irradiated skin tissues, we found that CXCL1 may negatively regulate melanogenesis. To validate this finding, we exogenously treated human primary melanocytes, MNT1 cells, and ex vivo human foreskin tissues with CXCL1. The results showed that CXCL1 reduced melanin content, tyrosinase activity, and the expression of key melanogenesis-related genes, including MITF, TYR, TYRP1, and DCT. Mechanistic studies revealed that CXCL1 exerts these inhibitory effects through its canonical receptor CXCR2. Notably, CXCL1 treatment significantly decreased both the expression level and nuclear translocation of β-catenin, a key effector molecule of the WNT signaling pathway, and this effect was effectively reversed by the specific CXCR2 inhibitor SB225002, suggesting that the CXCL1-CXCR2 axis negatively regulates melanogenesis by suppressing the WNT/β-catenin signaling pathway. In summary, this study elucidates a preliminary mechanism by which the CXCL1-CXCR2 axis negatively regulates melanogenesis through inhibition of the WNT/β-catenin signaling pathway, linking inflammatory cytokine networks to the regulatory machinery of melanogenesis. It provides novel perspectives for deciphering the pathogenesis of pigmentary skin disorders and developing therapeutic strategies with combined anti-inflammatory and depigmenting effects. - Source: PubMed
Publication date: 2026/07/31
Zhang YushanZhang FanYu XiaoyuanZhao XiaojiaoChen JingZhu JianjianKang Liyang - 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