PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27542283-4 2016 MARCKS upregulation was confirmed on protein level and also observed in other BTZ-resistant tumor cell lines as well as in leukemia cells with acquired resistance to other proteasome inhibitors. Bortezomib 78-81 myristoylated alanine rich protein kinase C substrate Homo sapiens 0-6 33668794-2 2021 The aim of our study is to assess the expression of previously described genes that may influence the resistance to bortezomib treatment at the mRNA level (ABCB1, CXCR4, MAF, MARCKS, POMP, PSMB5, RPL5, TXN, and XBP1) and prognosis of MM patients. Bortezomib 116-126 myristoylated alanine rich protein kinase C substrate Homo sapiens 175-181 27542283-5 2016 Moreover, when MARCKS protein expression was demonstrated in specimens derived from therapy-refractory pediatric leukemia patients (n = 44), higher MARCKS protein expression trended (p = 0.073) towards a dismal response to BTZ-containing chemotherapy. Bortezomib 223-226 myristoylated alanine rich protein kinase C substrate Homo sapiens 15-21 27542283-5 2016 Moreover, when MARCKS protein expression was demonstrated in specimens derived from therapy-refractory pediatric leukemia patients (n = 44), higher MARCKS protein expression trended (p = 0.073) towards a dismal response to BTZ-containing chemotherapy. Bortezomib 223-226 myristoylated alanine rich protein kinase C substrate Homo sapiens 148-154 27542283-6 2016 Mechanistically, we show a BTZ concentration-dependent association of MARCKS protein levels with the emergence of ubiquitin-containing vesicles in BTZ-resistant CEM cells. Bortezomib 27-30 myristoylated alanine rich protein kinase C substrate Homo sapiens 70-76 27542283-6 2016 Mechanistically, we show a BTZ concentration-dependent association of MARCKS protein levels with the emergence of ubiquitin-containing vesicles in BTZ-resistant CEM cells. Bortezomib 147-150 myristoylated alanine rich protein kinase C substrate Homo sapiens 70-76 27542283-8 2016 Consistent with these observations, MARCKS protein associated with ubiquitin-containing vesicles was also more prominent in clinical leukemic specimen with ex vivo BTZ resistance compared to BTZ-sensitive leukemia cells. Bortezomib 164-167 myristoylated alanine rich protein kinase C substrate Homo sapiens 36-42 27542283-8 2016 Consistent with these observations, MARCKS protein associated with ubiquitin-containing vesicles was also more prominent in clinical leukemic specimen with ex vivo BTZ resistance compared to BTZ-sensitive leukemia cells. Bortezomib 191-194 myristoylated alanine rich protein kinase C substrate Homo sapiens 36-42 27542283-9 2016 Collectively, we propose a role for MARCKS in a novel mechanism of BTZ resistance via exocytosis of ubiquitinated proteins in BTZ-resistant cells leading to quenching of proteolytic stress. Bortezomib 67-70 myristoylated alanine rich protein kinase C substrate Homo sapiens 36-42 27542283-9 2016 Collectively, we propose a role for MARCKS in a novel mechanism of BTZ resistance via exocytosis of ubiquitinated proteins in BTZ-resistant cells leading to quenching of proteolytic stress. Bortezomib 126-129 myristoylated alanine rich protein kinase C substrate Homo sapiens 36-42 25179733-5 2015 Functionally, inhibition of MARCKS phosphorylation by enzastaurin or knockdown of the gene by RNAi significantly enhanced the sensitivity of resistant HMCLs and primary MM samples to bortezomib and to other anti-myeloma drugs, providing evidence that MARCKS can modulate drug response. Bortezomib 183-193 myristoylated alanine rich protein kinase C substrate Homo sapiens 28-34 25179733-8 2015 Importantly, MARCKS knockdown in combination with bortezomib treatment overcame bortezomib resistance, significantly inhibited tumor growth and prolonged host survival in a MM xenograft model. Bortezomib 80-90 myristoylated alanine rich protein kinase C substrate Homo sapiens 13-19