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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- Vitex rotundifolia L.f. (VRL) is a plant belonging to the Verbenaceae family with antipyretic, analgesic, and anti-inflammatory properties, but research on the melanocyte-targeted skin depigmenting-related responses of VRL is lacking. In this study, VRL cone essential oil (VRLCEO) was obtained through steam distillation, and its effects on melanin synthesis and transport-related responses were investigated. Gas chromatography-mass spectrometry analysis identified 15 components from VRLCEO. In all biological activity experiments, VRLCEO was used at noncytotoxic concentrations (≤ 50 µg/mL) to ensure cell viability. VRLCEO inhibited serum-induced cell proliferation of B16BL6 mouse melanoma cells. VRLCEO suppressed tyrosinase enzyme activity and melanin synthesis in B16BL6 melanoma cells induced by α-MSH. VRLCEO also reduced the expression of MITF, tyrosinase, and TRP-2 proteins in α-melanocyte-stimulating hormone (α-MSH)-stimulated B16BL6 cells, but did not affect TRP-1 protein expression. Moreover, it increased the p38 MAPK and ERK1/2 phosphorylation levels in α-MSH-exposed B16BL6 cells, but not the JNK phosphorylation level. Furthermore, VRLCEO decreased α-MSH-upregulated Rab27a and melanophilin expression in B16BL6 cells. Therefore, VRLCEO may exert an anti-pigmentation effect by inhibiting melanin production and transfer in melanocytes. Accordingly, VRLCEO may be a natural material for the development of skin whitening agents. - Source: PubMed
Yoo Da YeonWon Kyung JongKim Yoon YiKim Do YoonBae Ji HyeYun Ji SeongLee Hwan Myung - Ultraviolet (UV) irradiation induces complex skin damage, including hyperpigmentation, oxidative stress, and alterations in proteins related to keratinocyte differentiation and epidermal barrier-associated status. This study investigated the multifunctional protective effects of ethanolic extract (PAEE) against skin damage in melanocytes, keratinocytes, and zebrafish. In alpha-melanocyte-stimulating hormone (α-MSH)-stimulated B16F10 cells, PAEE effectively suppressed the protein kinase A (PKA)/cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) signaling pathway, which was associated with reduced expression of microphthalmia-associated transcription factor (MITF) and tyrosinase, leading to decreased melanin synthesis. PAEE also exhibited photoprotective properties by reducing reactive oxygen species (ROS), inhibiting interleukin-1 beta (IL-1β), and attenuating matrix metalloproteinase-1 (MMP-1) upregulation associated with UVB (ultraviolet B)-induced photodamage in HaCaT keratinocytes. Notably, PAEE restored the UVB-reduced expression of filaggrin and involucrin, representative markers of keratinocyte differentiation and epidermal barrier-associated status, in HaCaT keratinocytes. In zebrafish embryos, PAEE suppressed α-MSH-induced melanin accumulation and UVB-induced ROS generation at non-toxic concentrations. Taken together, these results suggest that PAEE exerts anti-melanogenic and photoprotective effects in cellular and zebrasfish models and may serve as a promising marine-derived ingredient for cosmeceutical applications targeting UVB-related skin damage. - Source: PubMed
Publication date: 2026/04/09
Lee Yun-SuKim Wook-ChulLee Kyeong MinJung Seo-RinIm Seung TaeKang Min-CheolLee Seung-Hong - The aim of this study was to investigate the anti-melanogenic effects and underlying mechanisms of PFRMY (Pro-Phe-Arg-Met-Tyr), a pentapeptide derived from tilapia skin (), using B16F10 murine melanoma cells. Treatment with PFRMY (1.0 mg/mL) significantly reduced intracellular melanin content and tyrosinase (TYR) activity by 39.55 ± 1.51% and 32.46 ± 1.31%, respectively. RT-PCR and Western blotting analyses revealed that PFRMY suppressed melanogenesis through the α-MSH/PKA/CREB signaling pathway. Notably, PFRMY reversed α-MSH-induced upregulation of key downstream factors including PKA, CREB, MITF, and TYR, while showing minimal effects on the protein expression of MC1R or α-MSH. Molecular docking further suggested that PFRMY binds to MC1R with higher affinity than α-MSH, potentially occupying the ligand-binding site and thereby interfering with downstream signaling. Collectively, these findings demonstrate that PFRMY effectively inhibits melanogenesis by competitively antagonizing the α-MSH/MC1R axis, highlighting its potential as a safe and efficacious ingredient for hyperpigmentation treatment and cosmetic applications. - Source: PubMed
Publication date: 2026/04/15
Song YuqiongLu ChenChen ShengjunZhao YongqiangHuang HuiXiang HuanLong XiaoshanHu Xiao - Stereotactic body radiation therapy (SBRT) provides excellent local control for localized prostate cancer (PC); however, systemic relapse remains the primary cause of mortality in high-risk patients, underscoring the need to understand and therapeutically address radiation-induced immune suppression. Here, we identify a previously unrecognized myeloid checkpoint pathway driven by GPNMB⁺ myeloid-derived suppressor cells (MDSCs) as a dominant systemic response to clinical SBRT and demonstrate a tractable strategy to counter it. - Source: PubMed
Publication date: 2026/04/30
Mulvaney OscarChung Jin-SungKobayashi MasatoSomatilaka Bandarigoda GamagePop Laurentiu MZhang FayaCruz Ponciano DAriizumi KiyoshiHannan Raquibul - α-Melanocyte-stimulating hormone (α-MSH) is a key physiological inducer of melanogenesis and melanocyte activation. Reactive oxygen species (ROS) function as secondary messengers in intracellular signaling pathways that regulate α-MSH-mediated melanogenesis. However, the mechanism by which α-MSH induces ROS generation in melanocytes remains incompletely understood. Here, we investigated the sources and regulatory mechanisms of α-MSH-induced ROS in murine B16F10 and human MNT-1 melanoma cells. Confocal microscopy revealed that α-MSH predominantly stimulated cytosolic rather than mitochondrial ROS generation. Western blot analysis showed that α-MSH upregulated the expression of NADPH oxidases NOX1 and NOX4 at early time points, key enzymes involved in cytosolic ROS production. Pharmacological inhibition of NOX1/4 significantly reduced α-MSH-induced ROS levels and melanin content, accompanied by decreased phosphorylation of MITF, a melanogenic transcription factor. These findings indicate that α-MSH is a key physiological inducer of melanogenesis and melanocyte-related signaling in melanoma cells. Our study highlights NOX4, together with NOX1, as potential targets for anti-pigmentation strategies. - Source: PubMed
Publication date: 2026/04/30
Kim KyuriYoon JihyunKim Hye YeonLim Kyung-Min