Disease relevance of VPS11

• The peptides displayed by these phages were: pep1 = Ala-Asp-Gly-Gly-Ala-Gln-Gly-Thr-Ala; pep2 = Pro-Gly-Pro-Ser-Arg-Ala-His-Phe-Leu; pep3 = Leu-Ser-Ser-Arg-Glu-Pro-Gln-Ala-Arg; pep4 = Arg-Leu-Thr-Arg-Glu-Leu-Tyr-Ala-Gln and pep5 = Tyr-Thr-Gln-Lys-His-Gln-Ala [1].
• Expression of "Ia-like" antigens on cells from a human endometrial carcinoma cell line, END-1 [2].
• Our findings complement previous macroscale findings and are consistent with a cellular mechanism involving increased END1 and PDGFB levels, but decreased NOS3 levels, leading to intimal hyperplasia at regions of low magnitude reversing WSS [3].
• CONCLUSIONS: Our results show that gender and the END1 gene modify the phenotypic expression of hypertrophy in patients with HCM [4].
• The immunity mechanism of Pep5 in Staphylococcus epidermidis is based on inhibition of pore formation by a small 69-amino acid protein weakly associated with the outer surface of the cytoplasmic membrane [5].

High impact information on VPS11

• The protein products of hVPS11 (hVps11) and hVPS18 (hVps18) were ubiquitously expressed in peripheral tissues, suggesting that they have a fundamental role in cellular function [6].
• This study demonstrates altered receptor trafficking in End1 and End2 cell lines, a novel aspect of the mutant phenotypes [7].
• The lines (VK2/E6E7, Ect1/E6E7, and End1/E6E7) displayed distinctive morphologies at the level of light microscopy when cultured in calcium-supplemented (0.4 mM) keratinocyte serum-free medium and maintained a stable phenotype after more than 1 yr of continuous passage [8].
• The genotypes of AGT (M235T, T174M, and G-6A), AT1a, and END1 were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) or mutation-specific PCR (MS-PCR) [4].
• Heterozygous polymorphisms in the VPS11 and DPAGT1 genes were found [9].

Biological context of VPS11

• The END1 genotypes also had a significant influence on LVH scores accounting for 2.9% of their variability (p = 0.042) [4].
• A cluster of pathogenicity genes ( PEP1, PEP2, PDA1, PEP5), termed the pea pathogenicity ( PEP) cluster and located on a 1.6-Mb conditionally dispensable (CD) chromosome, was identified in the fungal pathogen Nectria haematococca [10].

Associations of VPS11 with chemical compounds

• They can be divided into unmodified peptides (e.g. lactococcins, lactacins, pediocins) and lanthionine-containing peptides (lantibiotics, e.g. nisin, epidermin, Pep5) [11].
• Training increased muscle ATP (P less than 0.05) and glycogen (P less than 0.01) concentrations and decreased muscle lactate concentration (P less than 0.05) in the TL at END1 [12].

References