PMEL Antibody

1. To provide a source of dual-specific T cells for ACT, we generated a transgenic mouse strain expressing a CAR specific for Her2 in leukocytes under the control of the vav promoter .This CAR mouse strain was bred onto the pMEL transgenic mouse strain, expressing a TCR specific for the premelanosome protein, gp100 PMID:27965307
2. IMCgp100 (ImmTAC recognizing a peptide derived from the melanoma-specific protein, gp100, presented by HLA-A*0201) efficiently redirects and activates effector and memory cells from both CD8(+) and CD4(+) repertoires to kill melanoma cells. PMID:28640942
3. our work attempts to provide structural insights into the RPT domain structure and to elucidate its contribution to Pmel17 amyloid fibril formation. PMID:26754844
4. These findings help to clarify the mechanism of T-cell recognition of gp100 during melanoma responses and could direct the development of altered peptides for vaccination. PMID:26917722
5. Data suggest that the Kringle-like domain of PMEL facilitates post-endoplasmic reticulum processing of disulfide-bonded PMEL dimers and promotes formation of PMEL functional amyloid fibrillar structures within multivesicular endosomes. PMID:26694611
6. mutant N-terminally extended peptides exhibited significantly increased HLA-A*02:01 binding affinity and elicited CD8(+) T cell stimulation in vitro similar to the wtgp100209-217 epitope. PMID:26507656
7. Data indicate that repeat domain (RPT) derived from Pmel17 aggregation kinetics were influenced only by lysolipid-containing phospholipid vesicles. PMID:25451784
8. Melanosome-autonomous regulation of size and number: the OA1 receptor sustains PMEL expression. PMID:24650003
9. SIL-TAL1 rearrangement identifies a distinct subtype with inferior outcome which could allow for individual therapeutic stratification for T-ALL patients. PMID:24040098
10. the molecular basis for the distinct trafficking and morphogenetic properties of PMEL and GPNMB is the PKD domain PMID:23452376
11. Data indicat that the N-terminal region of PMEL/Pmel17 is essential for the formation of melanosomal fibrils. PMID:23389629
12. BACE2 cleaves the integral membrane form of PMEL within the juxtamembrane domain, releasing the PMEL luminal domain into endosomal precursors for the formation of amyloid fibrils and downstream melanosome morphogenesis. PMID:23754390
13. The recombinant Pmel 17 plasmids were right as we expected by DNA sequencing PMID:23643172
14. The most significant single-nucleotide polymorphism in the 12q13.2 locus is located immediately upstream of the promoter region of PMEL for vitiligo in Han Chinese. PMID:22951725
15. An antibody drug conjugate reactive with PMEL17 exhibits target-dependent tumor cell killing in vitro and in vivo. PMID:22613716
16. This is a review on two human amyloidogenic polypeptides, one associated with Parkinson's disease, alpha-synuclein (alpha-syn), and the other important for melanin synthesis, the repeat domain (RPT) from Pmel17.[Review] PMID:21993592
17. MART-1- and gp100-expressing and -non-expressing melanoma cells are equally proliferative in tumors and clonogenic in vitro. PMID:21993558
18. Pmel17 repeat domain fibril dissolution is pH dependent PMID:22092386
19. the DW and HoSi mutations alter PMEL TMD oligomerization and/or association with membranes, with consequent formation of aberrantly packed fibrils. PMEL mutations can model the conversion between physiological and pathological amyloid PMID:21949659
20. the multistep processing of Pmel17 begins with an early cleavage during secretion that primes the protein for later functional processing. PMID:21247888
21. Repeat domains of melanosome matrix protein Pmel17 orthologs form amyloid fibrils at the acidic melanosomal pH. PMID:21148556
22. Data suggest that intramelanosomal pH regulates Pmel17 amyloid formation and its subsequent dissolution in vivo. PMID:21106765
23. N-terminal region and the polycystic kidney disease-like domain is highly crucial for endoplasmic reticulum export, subcellular targeting, and fibril formation by Pmel17 and thus for establishing functional melanosomes. PMID:20231267
24. Data conclude that sPmel17 is released by regulated proteolytic ectodomain shedding. PMID:19884326
25. we identified the gp100/pMel17 melanosomal protein as the shared antigen recognized by three independent CD8+ CTL clones in HLA-A*6801-restricted fashion. PMID:12135425
26. Data show that MITF appears to regulate the expression of the SILV and MLANA genes. PMID:12819038
27. 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 PMID:12925214
28. truncation of the repeat region within Pmel17 alters either fibrillogenic activity or the interaction of Pmel17 with melanin intermediates PMID:14632201
29. 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 PMID:15001714
30. PMEL17 is rapidly processed in the endoplasmic reticulum and glycosylated in the early Golgi PMID:15096515
31. Data suggest that MART-1 is indispensable for Pmel17 function and thus plays an important role in regulating mammalian pigmentation. PMID:15695812
32. 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. PMID:16516837
33. 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 PMID:16682408
34. Pmel17 is a critical component of melanogenesis. PMID:16704461
35. These data reveal a dual sorting defect in a natural mutant of Pmel17 and support a requirement of endocytic trafficking in Pmel17 fibril formation. PMID:16760433
36. addition of sialic acid affects the stability and sorting of Pmel17 and reduces pigmentation PMID:17303571
37. GTP-bound form of Rab7 promotes melanogenesis through the regulation of gp100 maturation in melanoma cells. PMID:17625594
38. Premelanosome amyloid-like fibrils are composed of only golgi-processed forms of Pmel17 that have been proteolytically processed in endosomes PMID:17991747
39. 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. PMID:18181974
40. Tyrosinase-, gp100-, or TRP-2-specific CD8(+) T cells could not be identified in the peripheral blood of individuals with vitiligo. PMID:18337837
41. Nuclear to non-nuclear Pmel17/gp100 expression (HMB45 staining) is a discriminator between benign and malignant melanocytic lesions. PMID:18552823
42. MHC class II presentation of gp100 epitopes in melanoma cells requires the function of conventional endosomes and is influenced by melanosomes. PMID:19017974
43. release of the Pmel17 ectodomain, which is critical for melanin amyloidogenesis, is initiated by S2 cleavage at a juxtamembrane position PMID:19047044
44. the repeat domain of the melanosome fibril protein Pmel17 forms the amyloid core promoting melanin synthesis PMID:19666488
45. N-terminal domains elicit formation of functional Pmel17 amyloid fibrils. PMID:19840945
46. Details and validates the multiple sorting pathways used by the silver protein to reach melanosomes. It identifies the specific adaptor proteins involved and sheds light on the polarization of the melanocyte. PMID:16492709
47. Detailed analysis of the post-translational modifications and their effect over the processing and trafficking of the silv gene. PMID:17303571
48. The PMEL17 (SILV) protein catalyzes the polymerization of 5,6-dihydroxyindole-2-carboxylic acid to melanin. PMID:8617263
49. Pmel17 is proteolytically processed in a post-Golgi compartment and is enriched in multivesicular endosomes prior to incorporation in stage II melanosomes. PMID:11694580
50. A proteolytic fragment of Pmel17, generated by proprotein convertase cleavage, is the major biogenetic component of the underlying fibrillar matrix of melanosome precursors. PMID:12732614

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HGNC: 10880

UNIGENE: Hs.95972

KEGG: hsa:6490

STRING: 9606.ENSP00000402758

OMIM: 155550