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Validated All-in-One™ qPCR Primer for PMEL(NM_001200054.1) Search again
Product ID:
HQP064816
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
D12S53E, HMB-45, HMB45, ME20, ME20-M, ME20M, P1, P100, PMEL17, SI, SIL, SILV, gp100
Gene Description:
premelanosome protein
Target Gene Accession:
NM_001200054.1(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Gene References into function
- The PMEL17 (SILV) protein catalyzes the polymerization of 5,6-dihydroxyindole-2-carboxylic acid to melanin.
- Pmel17 is proteolytically processed in a post-Golgi compartment and is enriched in multivesicular endosomes prior to incorporation in stage II melanosomes.
- we identified the gp100/pMel17 melanosomal protein as the shared antigen recognized by three independent CD8+ CTL clones in HLA-A*6801-restricted fashion.
- A proteolytic fragment of Pmel17, generated by proprotein convertase cleavage, is the major biogenetic component of the underlying fibrillar matrix of melanosome precursors.
- Data show that MITF appears to regulate the expression of the SILV and MLANA genes.
- Antigen-specific T lymphocyte reactivity to gp100 peptides was seen in 15 of 17 (88%) vitiligo patients, with many demonstrating very high reactivity at levels comparable with those observed with common recall antigens
- truncation of the repeat region within Pmel17 alters either fibrillogenic activity or the interaction of Pmel17 with melanin intermediates
- CD8 T lymphocytes recognized a nonameric peptide on melanoma cells that comprises two noncontiguous segments of melanocytic glycoprotein gp100(PMEL17); the production of this peptide involves the excision of four amino acids and splicing of the fragments
- PMEL17 is rapidly processed in the endoplasmic reticulum and glycosylated in the early Golgi
- Data suggest that MART-1 is indispensable for Pmel17 function and thus plays an important role in regulating mammalian pigmentation.
- Data show that the melanosomal protein Pmel17 is sorted into intralumenal vesicles by a mechanism that is dependent upon lumenal determinants and conserved in non-pigment cells.
- the RPT domain of PMEL17/GP100 is essential for its function in generating the fibrillar matrix of melanosomes and that the luminal domain is necessary for its correct processing and trafficking to those organelles
- Pmel17 is a critical component of melanogenesis.
- These data reveal a dual sorting defect in a natural mutant of Pmel17 and support a requirement of endocytic trafficking in Pmel17 fibril formation.
- addition of sialic acid affects the stability and sorting of Pmel17 and reduces pigmentation
- GTP-bound form of Rab7 promotes melanogenesis through the regulation of gp100 maturation in melanoma cells.
- Premelanosome amyloid-like fibrils are composed of only golgi-processed forms of Pmel17 that have been proteolytically processed in endosomes
- Measurement of Melan-A, gp100, MAGE-3, MIA and tyrosinase represents a prognostic factor and a method for early detection of metastasis and treatment response of melanoma patients.
- Tyrosinase-, gp100-, or TRP-2-specific CD8(+) T cells could not be identified in the peripheral blood of individuals with vitiligo.
- Nuclear to non-nuclear Pmel17/gp100 expression (HMB45 staining) is a discriminator between benign and malignant melanocytic lesions.
- MHC class II presentation of gp100 epitopes in melanoma cells requires the function of conventional endosomes and is influenced by melanosomes.
- release of the Pmel17 ectodomain, which is critical for melanin amyloidogenesis, is initiated by S2 cleavage at a juxtamembrane position