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PSMB5 mutations are associated with multiple myeloma.
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PSMB5 knockdown could increase the expression of pro-apoptosis gene Bax and cleaved caspase-3
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Our results suggest a potential role for PSMB5 as a biomarker and therapeutic target for Triple-negative breast cancer
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Results identified PSMB5 Q62P mutation to underlie bortezomib resistance in Down-syndrome-associated acute myeloid leukemia cells.
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We also discovered and replicated three genome-wide significant variants in previously unreported loci for RDW (SLC12A2 rs17764730, PSMB5 rs941718), and hematocrit (PROX1 rs3754140) and an upstream anti-sense long-noncoding RNA, LINC01184, as the likely causal variant
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Data indicate that proteasomal subunit X PSMB5 is a target of signal transducer and activator of transcription 3 (STAT3).
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Nuclear MB1 expression was an independent predictor of worse survival in ovarian cancer.
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critical role of PSMB5 in 20S proteasome-mediated protection against replicative senescence, pointing to a possible strategy for maintaining the integrity of culture-expanded bone marrow stromal cells by manipulating the expression of PSMB5
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The expression of proteasome beta5 decreases markedly in human atherosclerotic plaques.
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Data indicate that treatment-emergent resistance to single-agent bortezomib was independent of variants in the proteasome genes PSMB1, PSMB5, PSMB6, PSMB8, PSMB9, and PSMB10.
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Letter/Case Reports: proteasome subunit beta5t is expressed in cervical ectopic thymoma.
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PSMB5 overexpression is associated with Bortezomib resistance in myeloma.
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No mutations or differences in PSMB5 mRNA expression were seen before bortezomib treatment in 3 multiple myeloma patients, but after treatment, 1 patient showed PSMB5 upregulation associated with bortezomib resistance.
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CDK5 regulation of proteasome subunit PSMB5 was identified as a probable route to antineoplastic drug sensitization.
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Expression of mutated PSMB5 was associated with the prevention of the accumulation of unfolded proteins
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interaction of TAP1 and TAP2 and P-glycoprotein with proteasome subunits beta-5 and beta-5i suggest direct targeting of antigenic peptides to the ER via a TAP-proteasome association and a possible role for P-glycoprotein
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Proteasome activity can be genetically "upregulated" in lens cells by overexpression of beta5 catalytic subunit. Resulting increase in proteasome activity leads to decrease in oxidized proteins and enhanced cell survival following oxidative stress.
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G322A mutation of the PSMB5 gene is a novel mechanism for bortezomib resistance.
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nonsynonymous coding single nucleotide polymorphismsin the proteasome beta 5 subunit gene did not show significant effects on proteasome activity, but SNPs did influence transcription
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Overexpression of PSMB5 is an important mechanism for bortezomib resistance in Jurkat cell lines.
