The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis. - Wikidata - wikimedia - TriplyDB

The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis.

The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis.

http://www.wikidata.org/entity/Q35830099

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Structure of the Ire1 autophosphorylation complex and implications for the unfolded protein response Regulation of unfolded protein response modulator XBP1s by acetylation and deacetylation Blockade of XBP1 splicing by inhibition of IRE1α is a promising therapeutic option in multiple myeloma Divergent allosteric control of the IRE1α endoribonuclease using kinase inhibitors Identification of Toyocamycin, an agent cytotoxic for multiple myeloma cells, as a potent inhibitor of ER stress-induced XBP1 mRNA splicing Potent and selective inhibitors of the inositol-requiring enzyme 1 endoribonuclease Initial genome sequencing and analysis of multiple myeloma Prognostic significance of copy-number alterations in multiple myeloma XBP-1 regulates signal transduction, transcription factors and bone marrow colonization in B cells Cancer Microenvironment and Endoplasmic Reticulum Stress Response Factors regulating immunoglobulin production by normal and disease-associated plasma cells A novel mouse model for multiple myeloma (MOPC315.BM) that allows noninvasive spatiotemporal detection of osteolytic disease Divergent effects of PERK and IRE1 signaling on cell viability Structure of the Dual Enzyme Ire1 Reveals the Basis for Catalysis and Regulation in Nonconventional RNA Splicing Novel therapeutic strategies for multiple myeloma Inflammation and cellular stress: a mechanistic link between immune-mediated and metabolically driven pathologies Osteolytica: An automated image analysis software package that rapidly measures cancer-induced osteolytic lesions in in vivo models with greater reproducibility compared to other commonly used methods Characterization of a novel mouse model of multiple myeloma and its use in preclinical therapeutic assessment Mndal, a new interferon-inducible family member, is highly polymorphic, suppresses cell growth, and may modify plasmacytoma susceptibility Selective inhibition of tumor oncogenes by disruption of super-enhancers Molecular mechanisms of human IRE1 activation through dimerization and ligand binding (18)F-FDG-PET/CT imaging in an IL-6- and MYC-driven mouse model of human multiple myeloma affords objective evaluation of plasma cell tumor progression and therapeutic response to the proteasome inhibitor ixazomib.ER stress affects processing of MHC class I-associated peptides.Genetic variation of promoter sequence modulates XBP1 expression and genetic risk for vitiligo.A proto-oncogene BCL6 is up-regulated in the bone marrow microenvironment in multiple myeloma cells.The miR-125a and miR-320c are potential tumor suppressor microRNAs epigenetically silenced by the polycomb repressive complex 2 in multiple myeloma Regulation of basal cellular physiology by the homeostatic unfolded protein response XBP1 promotes triple-negative breast cancer by controlling the HIF1α pathway.The nuclear receptor peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) promotes oncogene-induced cellular senescence through repression of endoplasmic reticulum stress.Transgenic expression of entire hepatitis B virus in mice induces hepatocarcinogenesis independent of chronic liver injury Bone marrow microenvironment in myelomagenesis: its potential role in early diagnosis.Role of CAAT/enhancer binding protein homologous protein in panobinostat-mediated potentiation of bortezomib-induced lethal endoplasmic reticulum stress in mantle cell lymphoma cells.Endoplasmic reticulum stress is chronically activated in chronic pancreatitis Dinaciclib (SCH727965) inhibits the unfolded protein response through a CDK1- and 5-dependent mechanism Cancer stem cells: controversies in multiple myeloma Stimulation of surface IgM of chronic lymphocytic leukemia cells induces an unfolded protein response dependent on BTK and SYK.Dysregulation of unfolded protein response partially underlies proapoptotic activity of bortezomib in multiple myeloma cells.Enhancer alterations in cancer: a source for a cell identity crisis.Transcription factor MIST1 in terminal differentiation of mouse and human plasma cells.New insights, recent advances, and current challenges in the biological treatment of multiple myeloma.

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The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis.

http://www.wikidata.org/entity/Q35830099

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The differentiation and stress ...... multiple myeloma pathogenesis.

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The differentiation and stress ...... multiple myeloma pathogenesis.

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The differentiation and stress ...... multiple myeloma pathogenesis.

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Alexei Protopopov

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Daniel E Carrasco

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Daniel R Carrasco

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Elena V Ivanova

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Geraldine S Pinkus

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Giovanni Tonon

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James Horner

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Joel Henderson

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Kumar Sukhdeo

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Mala Mani

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P2860

Plasma cell differentiation requires the transcription factor XBP-1

Complementary signaling pathways regulate the unfolded protein response and are required for C. elegans development

High-resolution genomic profiles of human lung cancer

Significance analysis of microarrays applied to the ionizing radiation response

IRE1-mediated unconventional mRNA splicing and S2P-mediated ATF6 cleavage merge to regulate XBP1 in signaling the unfolded protein response

Proteasome inhibitors disrupt the unfolded protein response in myeloma cells

Expression of BCMA, TACI, and BAFF-R in multiple myeloma: a mechanism for growth and survival

IRE1 couples endoplasmic reticulum load to secretory capacity by processing the XBP-1 mRNA

Plasma cell differentiation and the unfolded protein response intersect at the transcription factor XBP-1

129-derived strains of mice are deficient in DNA polymerase iota and have normal immunoglobulin hypermutation

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349-360

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Kenneth C Anderson

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