Silver homologue _ Pmel 17

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Known as:: Silver homologue _ Pmel 17
Catalog number:: Y213561
Product Quantity:: 200ul
Category:: -
Supplier:: ABM
Gene target:: Silver homologue _ Pmel 17

Related genes to: Silver homologue _ Pmel 17

Gene:: PMEL ^{NIH gene}
Name:: premelanosome protein
Previous symbol:: SIL, SILV
Synonyms:: D12S53E, SI, Pmel17, gp100
Chromosome:: 12q13.2
Locus Type:: gene with protein product
Date approved:: 1997-06-24
Date modifiied:: 2016-06-10

Related products to: Silver homologue _ Pmel 17

Related articles to: Silver homologue _ Pmel 17

Aquaporin-5-specific heavy chain VDJ knock-in (A5H) mice reveal molecular mimicry-driven initiation and diversification of autoreactive B-cell responses.
Molecular mimicry, where microbial antigens resemble self-antigens, is implicated in triggering autoimmune responses, yet the early B-cell events leading to autoantibody production remain unclear. Here, we generated A5H mice, a knock-in model in which a heavy chain binding to the aquaporin-5 (AQP5) "E" epitope (AQP5E) preferentially generates B cells recognizing a microbial mimic peptide (PmE-L). A5H mice exhibited normal B-cell development with a phenotypic reduction in the anergy-associated B-cell compartment and an expanded pool of mimic-reactive B cells. At steady state, A5H mice produced anti-PmE-L antibodies, whereas anti-AQP5E autoantibodies were not detectable by ELISA. Upon immunization with PmE-L, mimic-reactive B cells were recruited into germinal center responses, leading to robust production of anti-AQP5E autoantibodies that cross-reacted with homologous AQPs (AQP4 and AQP1). Furthermore, A5H mice generated anti-AQP5E autoantibodies upon immunization with streptavidin-complexed PmE-L, indicating that A5H-derived mimic-reactive B cells can overcome competition with the immunodominant carrier antigen streptavidin. However, evidence of intramolecular epitope spreading to native AQP5 was not observed. Consistently, tissue deposition of autoantibodies and salivary gland pathology remained minimal. Notably, autoantibody responses were stronger in heterozygous (+/A5H) than homozygous (A5H/A5H) mice, indicating that allelic inclusion enhances autoreactive B-cell activation. These findings establish A5H mice as a valuable model to dissect how molecular mimicry initiates and diversifies autoreactive B-cell responses, advancing understanding of autoimmune disease initiation. - Source: PubMed
Publication date: 2026/07/02
Kim HyunjinLee NayoonAcharya SabinKim SungminChoi Youngnim
Recent cryo-EM structures redefine the functional amyloid landscape.
Amyloids are traditionally associated with neurodegenerative and systemic diseases, yet it is now clear that they also perform essential physiological functions across kingdoms of life. Over the last decade, advances in cryogenic electron microscopy (cryo-EM) have enabled high-resolution structural characterization of functional amyloids, transforming our understanding of how the amyloid fold can be repurposed for biological activity. A landmark study in 2020 reported the cryo-EM structure of Orb2, a neuronal amyloid required for long-term memory persistence, establishing the first atomic view of a nuclear amyloid fibril. Subsequent structures of human RNA-binding proteins that form functional amyloids further expanded this paradigm. The structure of hnRNPDL-2 revealed how prion-like low-complexity domains can assemble into highly ordered, stable fibrils while keeping the necessary functionality for RNA metabolism. More recently, cryo-EM structures of the pigment-associated amyloid PMEL have provided insight into the molecular basis of melanosome biogenesis and pigmentation. In parallel, structural studies of bacterial functional amyloids, including the biofilm protein FapC, have uncovered architectures optimized for mechanical robustness and environmental resilience. Together, these pioneering studies reveal shared structural principles, alongside organism-specific adaptations that distinguish functional amyloids from their pathological counterparts. - Source: PubMed
Publication date: 2026/04/02
Ventura SalvadorBartolomé-Nafría AndreaGarcia-Pardo Javier
Transcriptome Analysis Reveals a Follicular Microenvironment Melanogenesis Axis in Black-to-White Coat-Color Transition of Junken Meat Sheep.
Junken meat sheep exhibit a characteristic postnatal coat-color transition, in which the initially black fleece gradually fades and develops into a white-trunk phenotype; however, the transcriptional basis of this developmental change in follicular pigment output remains unclear. In this study, three Junken meat sheep lambs showing a natural postnatal black-to-white coat-color transition were sampled longitudinally at the newborn black-fleece stage and the 179-day white-trunk stage, generating three matched biological pairs for RNA-seq analysis. Representative candidate genes were further validated by RT-qPCR. Differential expression analysis identified 1657, 400, and 1086 differentially expressed genes in the C11 vs. C1, C22 vs. C2, and C33 vs. C3 comparisons, respectively. Functional enrichment analysis indicated that these genes were mainly associated with tyrosine metabolism, ECM-receptor interaction, focal adhesion, Phosphoinositide 3-kinase-Akt signaling pathway (PI3K-Akt), arachidonic acid metabolism, estrogen signaling, and immune-related pathways. Integrated analysis of shared downregulated genes and expression patterns highlighted candidate genes related to pigmentation, the ECM/follicular microenvironment, and regulatory or metabolic processes. Pigmentation-related genes, including , , , , and , were generally downregulated in 179-day white-trunk-stage skin, while changes in ECM- and metabolism-related genes suggested altered follicular microenvironmental regulation. These findings identify candidate transcriptional features associated with developmental coat-color fading in Junken meat sheep and support a follicular microenvironment-melanogenesis expression axis as a transcriptome-based framework for further investigation. - Source: PubMed
Publication date: 2026/06/30
Xi BinpengZhao SanchuanYu QianZhou HuaqianZhang WenzheChen YanCheng RuiqiWang ZhipengYang HuaLiu Jianbin
An anti-PMEL antibody-drug conjugate with a G inhibitor payload in GNAQ/GNA11-mutant melanomas: a phase 1 trial.
Metastatic uveal melanoma (mUM) is an aggressive cancer with limited treatment options; 85-90% of tumors harbor activating GNAQ and GNA11 mutations. Uveal melanoma cells also express PMEL (also known as PMEL17 or gp100), a melanocyte lineage antigen. DYP688, a novel biology-matched antibody-drug conjugate, binds surface PMEL and delivers the potent Gα/Gα (G) inhibitor SDZ475 as payload by internalization. This dose-escalating first-in-human phase 1 study of DYP688 in patients with metastatic uveal melanoma and other GNAQ/GNA11-mutant melanomas assessed safety as the primary endpoint and pharmacokinetics and preliminary antitumor activity as secondary endpoints. Sixty-six patients received varying DYP688 doses and schedules. Grade 3 treatment-related adverse events occurred in five patients (7.6%), including one dose-limiting toxicity of grade 3 hypotension. Objective responses were seen in 13 out of 66 patients (19.7%) and tumor reduction in 47 out of 66 patients (71.2%). Median progression-free survival was 7.2 (95% CI: 5.3-7.8) months. In summary, DYP688 was well tolerated and showed preliminary efficacy, supporting this novel therapeutic approach. ClinicalTrials.gov identifier: NCT05415072 . - Source: PubMed
Publication date: 2026/07/13
Carlino Matteo SKapiteijn EllenPiperno-Neumann SophieSullivan Ryan JCarvajal RichardDummer ReinhardGromke TanjaHassel Jessica CKee DamienRamelyte EgleShoushtari Alexander NWei Alexander ZEnk AlexanderHandel Eleanor EMontazeri KamanehRamon-Patino JorgeRichly HeikeRodrigues ManuelSandhu ShahneenSmithy JamesSpeetjens Frank MMilanez-Almeida PedroChaudhury AnweshaHoffmaster KeithIsing MaryOtero Javier ARamKumar ThiruvamoorReynolds AimeeSharaby SherifWerner LillianYerramilli-Rao PadmajaCalvo Emiliano
Tinosporide promotes melanogenesis via activation of cAMP/PKA/CREB-MITF signaling in B16F10 and SK-MEL-2 cells.
Hypopigmentation disorders are characterized by impaired melanogenesis and remain challenging to manage due to limited efficacy of current interventions and insufficient mechanistic insights. Natural products represent a valuable source of bioactive phytoconstituents capable of regulating key pathways involved in melanin synthesis. Despite its extensive traditional use and diverse pharmacological activities, Tinospora cordifolia and its major bioactive constituent tinosporide remain unexplored for their role in melanogenesis. The present study aimed to evaluate the melanogenesis-promoting potential of bioactive phytoconstituents isolated from Tinospora cordifolia, and to elucidate their underlying molecular mechanisms. Four phytoconstituents-columbin, tinosporide, 8-hydroxy tinosporide and ecdysterone-were isolated and structurally characterized from T. cordifolia. Their melanogenic potential was evaluated in murine (B16F10) and human (SK-MEL-2) melanoma cells by assessing melanin content, tyrosinase activity, and expression of melanogenesis-associated genes. Intracellular cAMP levels and associated signalling pathways were further analysed to investigate the mechanism of action. Among the isolated compounds, tinosporide exhibited the most pronounced melanogenic activity, significantly increasing melanin synthesis and tyrosinase activity. Tinosporide promotes nuclear localization of the microphthalmia-associated transcription factor (MITF), leading to upregulation of MITF-target genes, including Trp1, Tyr, Dct, Pmel, and Mlana. Furthermore, mechanistic studies revealed that tinosporide elevated intracellular cAMP levels and induced the phosphorylation of PKA and CREB, thereby activating cAMP/PKA/CREB signalling pathway. Pharmacological inhibition of PKA and CREB markedly attenuated tinosporide-induced melanogenesis, confirming the essential role of the cAMP/PKA/CREB-MITF axis. Collectively, these findings identify tinosporide as a promising natural melanogenic agent derived from Tinospora cordifolia and highlight its potential relevance in the development of plant-based interventions for hypopigmentation disorders. - Source: PubMed
Publication date: 2026/06/30
Dhabal SukhamoyChakrabarty Anirban KrRai Rajiva KumarMohapatra SatyabrataSingh RahulKatiyar Chandra KantDubey Sunil Kumar

Silver homologue _ Pmel 17

Related genes to: Silver homologue _ Pmel 17

Related products to: Silver homologue _ Pmel 17

Related articles to: Silver homologue _ Pmel 17

Aquaporin-5-specific heavy chain VDJ knock-in (A5H) mice reveal molecular mimicry-driven initiation and diversification of autoreactive B-cell responses.

Recent cryo-EM structures redefine the functional amyloid landscape.

Transcriptome Analysis Reveals a Follicular Microenvironment Melanogenesis Axis in Black-to-White Coat-Color Transition of Junken Meat Sheep.

An anti-PMEL antibody-drug conjugate with a G inhibitor payload in GNAQ/GNA11-mutant melanomas: a phase 1 trial.

Tinosporide promotes melanogenesis via activation of cAMP/PKA/CREB-MITF signaling in B16F10 and SK-MEL-2 cells.