XBP1, Downstream of Blimp-1, Expands the Secretory Apparatus and Other Organelles, and Increases Protein Synthesis in Plasma Cell Differentiation

Shaffer, Arthur L.; Shelef, Miriam A.; Iwakoshi, Neal N.; Lee, Ann–Hwee; Qian, Shu‐Bing; Zhao, Hong; Yu, Xin; Yang, Liming; Tan, Bruce K.; Rosenwald, Andreas; Hurt, Elaine M.; Petroulakis, Emmanuel; Sonenberg, Nahum; Yewdell, Jonathan W.; Calame, Kathryn; Glimcher, Laurie H.; Staudt, Louis M.

doi:10.1016/j.immuni.2004.06.010

Cited by 902 publications

(962 citation statements)

References 69 publications

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“…This signature is in accordance with a known distinctive feature of AIL lesions, which is the presence of an expanded B-cell population (Dogan et al, 2003). Overexpression of XBP1 suggests that this transcription factor could play a role in the development of B-cell hyperplasia in AIL lesions, since it is known to be a crucial factor influencing B-cell and plasma cell differentiation (Chauhan et al, 2003;Munshi et al, 2004;Shaffer et al, 2004). RUNX1 may also be related to AIL pathogenesis, since it is known to be often overexpressed in acute leukemia (Cameron and Neil, 2004).…”

Section: T-cell Lymphoma Gene Expression Profiling B Ballester Et Alsupporting

confidence: 81%

Gene expression profiling identifies molecular subgroups among nodal peripheral T-cell lymphomas

et al. 2005

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Section: T-cell Lymphoma Gene Expression Profiling B Ballester Et Alsupporting

confidence: 81%

Gene expression profiling identifies molecular subgroups among nodal peripheral T-cell lymphomas

et al. 2005

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“…Genes encoding ER proteins were identified by database annotation, and the number of candidate genes was subsequently increased by literature search and use of algorithms predicting ER localization. This approach identified several genes that were previously shown to encode XBP-1 targets, including p58 IPK /DNAJC3, ERdj4/DNAJB9, ERdj5/DNAJC10, ERdj3/HEDJ, EDEM, PDIA4/ERP70, PDIA6/PDI-P5, PDIR, and RAMP4/SERP1 (Lee et al, 2003;Shaffer et al, 2004). Thus, ectopic expression of a lung-specific, mutant, nonglycosylated, membrane protein (SP-C ⌬exon4 or SP-C L188Q ) in embryonic kidney cells induced a subset of genes that was also associated with ER stress induced by tunicamycin or DTT.…”

Section: Discussionmentioning

confidence: 99%

ERdj4 and ERdj5 Are Required for Endoplasmic Reticulum-associated Protein Degradation of Misfolded Surfactant Protein C

Dong

Bridges

Apsley

et al. 2008

MBoC

142

171

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Mutations in the SFTPC gene associated with interstitial lung disease in human patients result in misfolding, endoplasmic reticulum (ER) retention, and degradation of the encoded surfactant protein C (SP-C) proprotein. In this study, genes specifically induced in response to transient expression of two disease-associated mutations were identified by microarray analyses. Immunoglobulin heavy chain binding protein (BiP) and two heat shock protein 40 family members, endoplasmic reticulum-localized DnaJ homologues ERdj4 and ERdj5, were significantly elevated and exhibited prolonged and specific association with the misfolded proprotein; in contrast, ERdj3 interacted with BiP, but it did not associate with either wild-type or mutant SP-C. Misfolded SP-C, ERdj4, and ERdj5 coprecipitated with p97/VCP indicating that the cochaperones remain associated with the misfolded proprotein until it is dislocated to the cytosol. Knockdown of ERdj4 and ERdj5 expression increased ER retention and inhibited degradation of misfolded SP-C, but it had little effect on the wild-type protein. Transient expression of ERdj4 and ERdj5 in X-box binding protein 1 ؊/؊ mouse embryonic fibroblasts substantially restored rapid degradation of mutant SP-C proprotein, whereas transfection of HPD mutants failed to rescue SP-C endoplasmic reticulum-associated protein degradation. ERdj4 and ERdj5 promote turnover of misfolded SP-C and this activity is dependent on their ability to stimulate BiP ATPase activity.

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“…OBF1 and Aiolos are crucial for the transition of pre-B cells to immature B cells expressing BCR, as well as for the mobilization of immature B-cells from bone marrow to the spleen, whereas NF-κB activation has essential roles in the transition of immature to mature B-cells [171][172][173] . Additionally, BCL6, IRF4, BLIMP1, XBP1 and PAX5 are involved in the terminal differentiation of B-cells into plasma cells [174][175][176][177][178][179][180][181][182] .…”

Section: Do Lymphoid Malignancies Arise From Mutations That Deregulatmentioning

confidence: 99%

Somatic stem cells and the origin of cancer

2006

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647Most human cancers derive from a single cell targeted by genetic and epigenetic alterations that initiate malignant transformation. Progressively, these early cancer cells give rise to different generations of daughter cells that accumulate additional mutations, acting in concert to drive the full neoplastic phenotype 1,2 . As we have currently deciphered many of the gene pathways disrupted in cancer, our knowledge about the nature of the normal cells susceptible to transformation upon mutation has remained more elusive. Adult stem cells are those that show long-term replicative potential, together with the capacities of self-renewal and multi-lineage differentiation. These stem cell properties are tightly regulated in normal development, yet their alteration may be a critical issue for tumorigenesis. This concept has arisen from the striking degree of similarity noted between somatic stem cells and cancer cells, including the fundamental abilities to self-renew and differentiate. Given these shared attributes, it has been proposed that cancers are caused by transforming mutations occurring in tissue-specific stem cells 3-9 . This hypothesis has been functionally supported by the observation that among all cancer cells within a particular tumor, only a minute cell fraction has the exclusive potential to regenerate the entire tumor cell population 3,10-13 ; these cells with stem-like properties have been termed cancer stem cells. Cancer stem cells can originate from mutation in normal somatic stem cells that deregulate their physiological programs. Alternatively, mutations may target more committed progenitor cells or even mature cells, which become reprogrammed to acquire stem-like functions 14,15 In any case, mutated genes should promote expansion of stem/progenitor cells, thus increasing their predisposition to cancer development by expanding self-renewal and pluripotency over their normal tendency towards relative quiescency and proper differentiation.

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XBP1, Downstream of Blimp-1, Expands the Secretory Apparatus and Other Organelles, and Increases Protein Synthesis in Plasma Cell Differentiation

Cited by 902 publications

References 69 publications

Gene expression profiling identifies molecular subgroups among nodal peripheral T-cell lymphomas

Gene expression profiling identifies molecular subgroups among nodal peripheral T-cell lymphomas

ERdj4 and ERdj5 Are Required for Endoplasmic Reticulum-associated Protein Degradation of Misfolded Surfactant Protein C

Somatic stem cells and the origin of cancer

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