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[PMID]: 24986674
[Au] Autor:Chopra R; Shakkottai VG
[Ad] Address:Department of Neurology, University of Michigan, 109 Zina Pitcher Place, Ann Arbor, MI, 48109-2200, USA.
[Ti] Title:The role for alterations in neuronal activity in the pathogenesis of polyglutamine repeat disorders.
[So] Source:Neurotherapeutics;11(4):751-63, 2014 Oct.
[Is] ISSN:1878-7479
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Polyglutamine diseases are a class of neurodegenerative diseases that share an expansion of a glutamine-encoding CAG tract in the respective disease genes as a central hallmark. In all of these diseases there is progressive degeneration in a select subset of neurons, and the mechanisms behind this degeneration remain unclear. Emerging evidence from animal models of disease has identified abnormalities in synaptic signaling and intrinsic excitability in affected neurons, which coincide with the onset of symptoms and precede apparent neuropathology. The appearance of these early changes suggests that altered neuronal activity might be an important component of network dysfunction and that these alterations in network physiology could contribute to symptoms of disease. Here we review abnormalities in neuronal function that have been identified in both animal models and patients, and highlight ways in which these changes in neuronal activity may contribute to disease symptoms. We then review the literature supporting an emerging role for abnormalities in neuronal activity as a driver of neurodegeneration. Finally, we identify common themes that emerge from studies of neuronal dysfunction in polyglutamine disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s13311-014-0289-7

  2 / 4006362 MEDLINE  
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[PMID]: 24778086
[Au] Autor:Arvold ND; Wang Y; Zigler C; Schrag D; Dominici F
[Ad] Address:Department of Radiation Oncology, Dana-Farber/Brigham & Women's Hospital, Boston, Massachusetts (N.D.A.); Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts (Y.W., C.Z., F.D.); Department of Medicine, Dana-Farber Cancer Institute, Boston, Massachusetts (D.S.)....
[Ti] Title:Hospitalization burden and survival among older glioblastoma patients†.
[So] Source:Neuro Oncol;16(11):1530-40, 2014 Nov.
[Is] ISSN:1523-5866
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Half of all glioblastoma patients are at least 65 years old. The frequency and duration of hospitalization from disease- and treatment-related morbidity in this population are unknown. METHODS: We performed a retrospective cohort study among patients aged 65 years and older with glioblastoma diagnosed between 1999 and 2007 using SEER-Medicare linked data. Diagnoses and procedures were identified using administrative claims data. Logistic regression was performed to identify predictors of high hospitalization burden. RESULTS: Among the 5029 patients in the cohort, 52% were ages 65-74, and 52% were male. Twenty-six percent of patients underwent extensive resection, 72% received radiotherapy, and 18% received temozolomide. Median survival was 4.9 months. Among all patients, 21% were hospitalized at least 30 cumulative days between diagnosis and death, and 22% of all patients spent at least one-fourth of their remaining lives as inpatients. Higher comorbidity score (adjusted hazard ratio [AHR], 1.72; 95% CI, 1.42-2.07) and black race (AHR, 1.56; 95% CI, 1.11-2.18) were associated with an increased risk of being hospitalized for at least 25% of remaining life, whereas radiation (AHR, 0.49; 95% CI, 0.42-0.58), temozolomide (AHR, 0.31; 95% CI, 0.23-0.42), and extensive surgery (AHR, 0.83; 95% CI, 0.69-0.99) were associated with a decreased risk. CONCLUSIONS: These data highlight the burden of hospitalization faced by a large proportion of older glioblastoma patients. In the setting of short survival, strategies to reduce the amount of time these patients spend hospitalized are urgently needed, to help maintain quality of life at the end of life.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1093/neuonc/nou060

  3 / 4006362 MEDLINE  
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[PMID]: 25256709
[Au] Autor:Bodenstine TM; Seftor RE; Seftor EA; Khalkhali-Ellis Z; Samii NA; Monarrez JC; Chandler GS; Pemberton PA; Hendrix MJ
[Ad] Address:Stanley Manne Children's Research Institute, Cancer Biology and Epigenomics Program, Northwestern University Feinberg School of Medicine, Robert H. Lurie Comprehensive Cancer Center, Chicago, Illinois....
[Ti] Title:Internalization by multiple endocytic pathways and lysosomal processing impact maspin-based therapeutics.
[So] Source:Mol Cancer Res;12(10):1480-91, 2014 Oct.
[Is] ISSN:1557-3125
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:UNLABELLED: Patients with metastatic disease face high rates of mortality with a paucity of therapeutic options. Protein-based therapeutics provide advantages over traditional chemotherapy through increased specificity, decreased immune impairment, and more direct means of delivery. However, development is often hindered because of insufficient knowledge about protein processing by cells when exogenously applied. This study focuses on recombinant Maspin (rMaspin), a serine protease inhibitor (SERPINB5), which alters invasive properties when directly applied to cancer cells. Previous evidence suggests differences in the effects of rMaspin treatment when compared with endogenous reexpression, with little explanation for these discrepancies. A leading hypothesis is that exogenously applied rMaspin is subject to different regulatory and/or processing mechanisms in cancer cells when compared with endogenous expression. Therefore, a more detailed understanding of the mechanisms of internalization and subcellular trafficking of rMaspin is needed to guide future translational development. We describe the molecular trafficking of rMaspin in cytoplasmic vesicles of the endosomal/lysosomal pathway and characterize its uptake by multiple endocytic mechanisms. Time-lapse laser scanning confocal microscopy shows the uptake, in real time, of dye-labeled rMaspin in cancer cells. This study indicates that cellular processing of rMaspin plays a key role by affecting its biologic activity and highlights the need for new approaches aimed at increasing the availability of rMaspin when used to treat cancer. IMPLICATIONS: Novel characterization of internalization and subcellular trafficking of rMaspin provides new insights for future therapeutic development. Mol Cancer Res; 12(10); 1480-91. ©2014 AACR.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1158/1541-7786.MCR-14-0067

  4 / 4006362 MEDLINE  
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[PMID]: 24966347
[Au] Autor:Marek LA; Hinz TK; von Mässenhausen A; Olszewski KA; Kleczko EK; Boehm D; Weiser-Evans MC; Nemenoff RA; Hoffmann H; Warth A; Gozgit JM; Perner S; Heasley LE
[Ad] Address:Department of Craniofacial Biology, University of Colorado Anschutz Medical Campus, Aurora, Colorado....
[Ti] Title:Nonamplified FGFR1 Is a Growth Driver in Malignant Pleural Mesothelioma.
[So] Source:Mol Cancer Res;12(10):1460-9, 2014 Oct.
[Is] ISSN:1557-3125
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:UNLABELLED: Malignant pleural mesothelioma (MPM) is associated with asbestos exposure and is a cancer that has not been significantly affected by small molecule-based targeted therapeutics. Previously, we demonstrated the existence of functional subsets of lung cancer and head and neck squamous cell carcinoma (HNSCC) cell lines in which fibroblast growth factor receptor (FGFR) autocrine signaling functions as a nonmutated growth pathway. In a panel of pleural mesothelioma cell lines, FGFR1 and FGF2 were coexpressed in three of seven cell lines and were significantly associated with sensitivity to the FGFR-active tyrosine kinase inhibitor (TKI), ponatinib, both in vitro and in vivo using orthotopically propagated xenografts. Furthermore, RNAi-mediated silencing confirmed the requirement for FGFR1 in specific mesothelioma cells and sensitivity to the FGF ligand trap, FP-1039, validated the requirement for autocrine FGFs. None of the FGFR1-dependent mesothelioma cells exhibited increased FGFR1 gene copy number, based on a FISH assay, indicating that increased FGFR1 transcript and protein expression were not mediated by gene amplification. Elevated FGFR1 mRNA was detected in a subset of primary MPM clinical specimens and like MPM cells; none harbored increased FGFR1 gene copy number. These results indicate that autocrine signaling through FGFR1 represents a targetable therapeutic pathway in MPM and that biomarkers distinct from increased FGFR1 gene copy number such as FGFR1 mRNA would be required to identify patients with MPM bearing tumors driven by FGFR1 activity. IMPLICATIONS: FGFR1 is a viable therapeutic target in a subset of MPMs, but FGFR TKI-responsive tumors will need to be selected by a biomarker distinct from increased FGFR1 gene copy number, possibly FGFR1 mRNA or protein levels. Mol Cancer Res; 12(10); 1460-9. ©2014 AACR.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1158/1541-7786.MCR-14-0038

  5 / 4006362 MEDLINE  
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[PMID]: 25274529
[Au] Autor:Collins E; Gu F; Qi M; Molano I; Ruiz P; Sun L; Gilkeson GS
[Ad] Address:Division of Rheumatology and Immunology, Department of Medicine, Medical University of South Carolina, Charleston, SC 29425; collinel@musc.edu....
[Ti] Title:Differential efficacy of human mesenchymal stem cells based on source of origin.
[So] Source:J Immunol;193(9):4381-90, 2014 Nov 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Mesenchymal stem cells (MSCs) are useful in tissue repair but also possess immunomodulatory properties. Murine and uncontrolled human trials suggest efficacy of MSCs in treating lupus. Autologous cells are preferable; however, recent studies suggest that lupus-derived MSCs lack efficacy in treating disease. Thus, the optimum derivation of MSCs for use in lupus is unknown. It is also unknown which in vitro assays of MSC function predict in vivo efficacy. The objectives for this study were to provide insight into the optimum source of MSCs and to identify in vitro assays that predict in vivo efficacy. We derived MSCs from four umbilical cords, four healthy bone marrows (BMs), and four lupus BMs. In diseased MRL/lpr mice, MSCs from healthy BM and umbilical cords significantly decreased renal disease, whereas lupus BM MSCs only delayed disease. Current in vitro assays did not differentiate efficacy of the different MSCs. However, differences in MSC efficacy were observed in B cell proliferation assays. Our results suggest that autologous MSCs from lupus patients are not effective in treating disease. Furthermore, standard in vitro assays for MSC licensing are not predictive of in vivo efficacy, whereas inhibiting B cell proliferation appears to differentiate effective MSCs from ineffective MSCs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1401636

  6 / 4006362 MEDLINE  
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[PMID]: 25267975
[Au] Autor:Wen Z; Fan L; Li Y; Zou Z; Scott MJ; Xiao G; Li S; Billiar TR; Wilson MA; Shi X; Fan J
[Ad] Address:Department of Anesthesiology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China; Department of Anesthesiology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China; Department of Surgery, University of Pittsburgh School of Medicine, ...
[Ti] Title:Neutrophils counteract autophagy-mediated anti-inflammatory mechanisms in alveolar macrophage: role in posthemorrhagic shock acute lung inflammation.
[So] Source:J Immunol;193(9):4623-33, 2014 Nov 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Acute lung injury (ALI) is a major component of multiple organ dysfunction syndrome after hemorrhagic shock (HS) resulting from major surgery and trauma. The increased susceptibility in HS patients to the development of ALI suggests not yet fully elucidated mechanisms that enhance proinflammatory responses and/or suppress anti-inflammatory responses in the lung. Alveolar macrophages (AMϕ) are at the center of the pathogenesis of ALI after HS. We have previously reported that HS-activated polymorphonuclear neutrophils (PMNs) interact with macrophages to influence inflammation progress. In this study, we explore a novel function of PMNs regulating AMϕ anti-inflammatory mechanisms involving autophagy. Using a mouse "two-hit" model of HS/resuscitation followed by intratracheal injection of muramyl dipeptide, we demonstrate that HS initiates high mobility group box 1/TLR4 signaling, which upregulates NOD2 expression in AMϕ and sensitizes them to subsequent NOD2 ligand muramyl dipeptide to augment lung inflammation. In addition, upregulated NOD2 signaling induces autophagy in AMϕ, which negatively regulates lung inflammation through feedback suppression of NOD2-RIP2 signaling and inflammasome activation. Importantly, we further demonstrate that HS-activated PMNs that migrate in alveoli counteract the anti-inflammatory effect of autophagy in AMϕ, possibly through NAD(P)H oxidase-mediated signaling to enhance I-κB kinase γ phosphorylation, NF-κB activation, and nucleotide-binding oligomerization domain protein 3 inflammasome activation, and therefore augment post-HS lung inflammation. These findings explore a previously unidentified complexity in the mechanisms of ALI, which involves cell-cell interaction and receptor cross talk.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1400899

  7 / 4006362 MEDLINE  
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[PMID]: 25225671
[Au] Autor:McLaughlin KA; Gulati K; Richardson CC; Morgan D; Bodansky HJ; Feltbower RG; Christie MR
[Ad] Address:Division of Diabetes and Nutritional Sciences, Guy's Campus, King's College London, London SE1 1UL, United Kingdom; and....
[Ti] Title:HLA-DR4-Associated T and B Cell Responses to Specific Determinants on the IA-2 Autoantigen in Type 1 Diabetes.
[So] Source:J Immunol;193(9):4448-56, 2014 Nov 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Autoantibodies to IA-2 in type 1 diabetes are associated with HLA-DR4, suggesting influences of HLA-DR4-restricted T cells on IA-2-specific B cell responses. The aim of this study was to investigate possible T-B cell collaboration by determining whether autoantibodies to IA-2 epitopes are associated with T cell responses to IA-2 peptides presented by DR4. T cells secreting the cytokines IFN-γ and IL-10 in response to seven peptides known to elicit T cell responses in type 1 diabetes were quantified by cytokine ELISPOT in HLA-typed patients characterized for Abs to IA-2 epitopes. T cell responses were detected to all peptides tested, but only IL-10 responses to 841-860 and 853-872 peptides were associated with DR4. Phenotyping by RT-PCR of FACS-sorted CD45RO(hi) T cells secreting IL-10 in response to these two peptides indicated that these expressed GATA-3 or T-bet, but not FOXP3, consistent with these being Th2 or Th1 memory T cells rather than of regulatory phenotype. T cell responses to the same two peptides were also associated with specific Abs: those to 841-860 peptide with Abs to juxtamembrane epitopes, which appear early in prediabetes, and those to peptide 853-872 with Abs to an epitope located in the 831-862 central region of the IA-2 tyrosine phosphatase domain. Abs to juxtamembrane and central region constructs were both DR4 associated. This study identifies a region of focus for B and T cell responses to IA-2 in HLA-DR4 diabetic patients that may explain HLA associations of IA-2 autoantibodies, and this region may provide a target for future immune intervention to prevent disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1301902

  8 / 4006362 MEDLINE  
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[PMID]: 25199761
[Au] Autor:Basch E; Loblaw DA; Oliver TK; Carducci M; Chen RC; Frame JN; Garrels K; Hotte S; Kattan MW; Raghavan D; Saad F; Taplin ME; Walker-Dilks C; Williams J; Winquist E; Bennett CL; Wootton T; Rumble RB; Dusetzina SB; Virgo KS
[Ad] Address:Ethan Basch, Ronald C. Chen, and Stacie B. Dusetzina, University of North Carolina, Chapel Hill; Derek Raghavan, Carolinas Health Care/Levine Cancer Institute, Charlotte, NC; D. Andrew Loblaw, Odette Cancer Centre, Sunnybrook Health Sciences Centre; Ted Wootton, Patient Representatives, Toronto; Seb...
[Ti] Title:Systemic therapy in men with metastatic castration-resistant prostate cancer: american society of clinical oncology and cancer care ontario clinical practice guideline.
[So] Source:J Clin Oncol;32(30):3436-48, 2014 Oct 20.
[Is] ISSN:1527-7755
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: To provide treatment recommendations for men with metastatic castration-resistant prostate cancer (CRPC). METHODS: The American Society of Clinical Oncology and Cancer Care Ontario convened an expert panel to develop evidence-based recommendations informed by a systematic review of the literature. RESULTS: When added to androgen deprivation, therapies demonstrating improved survival, improved quality of life (QOL), and favorable benefit-harm balance include abiraterone acetate/prednisone, enzalutamide, and radium-223 ((223)Ra; for men with predominantly bone metastases). Improved survival and QOL with moderate toxicity risk are associated with docetaxel/prednisone. For asymptomatic/minimally symptomatic men, improved survival with unclear QOL impact and low toxicity are associated with sipuleucel-T. For men who previously received docetaxel, improved survival, unclear QOL impact, and moderate to high toxicity risk are associated with cabazitaxel/prednisone. Modest QOL benefit (without survival benefit) and high toxicity risk are associated with mitoxantrone/prednisone after docetaxel. No benefit and excess toxicity are observed with bevacizumab, estramustine, and sunitinib. RECOMMENDATIONS: Continue androgen deprivation (pharmaceutical or surgical) indefinitely. Abiraterone acetate/prednisone, enzalutamide, or (223)Ra should be offered; docetaxel/prednisone should also be offered, accompanied by discussion of toxicity risk. Sipuleucel-T may be offered to asymptomatic/minimally symptomatic men. For men who have experienced progression with docetaxel, cabazitaxel may be offered, accompanied by discussion of toxicity risk. Mitoxantrone may be offered, accompanied by discussion of limited clinical benefit and toxicity risk. Ketoconazole or antiandrogens (eg, bicalutamide, flutamide, nilutamide) may be offered, accompanied by discussion of limited known clinical benefit. Bevacizumab, estramustine, and sunitinib should not be offered. There is insufficient evidence to evaluate optimal sequences or combinations of therapies. Palliative care should be offered to all patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1200/JCO.2013.54.8404

  9 / 4006362 MEDLINE  
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[PMID]: 25204659
[Au] Autor:Mobasher MA; de Toro-Martín J; González-Rodríguez A; Ramos S; Letzig LG; James LP; Muntané J; Alvarez C; Valverde AM
[Ad] Address:From the Instituto de Investigaciones Biomédicas Alberto Sols (CSIC-UAM), 28029 Madrid, Spain, the Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Instituto de Salid Carlos III, 28029 Madrid....
[Ti] Title:Essential Role of Protein-tyrosine Phosphatase 1B in the Modulation of Insulin Signaling by Acetaminophen in Hepatocytes.
[So] Source:J Biol Chem;289(42):29406-19, 2014 Oct 17.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Many drugs are associated with the development of glucose intolerance or deterioration in glycemic control in patients with pre-existing diabetes. We have evaluated the cross-talk between signaling pathways activated by acetaminophen (APAP) and insulin signaling in hepatocytes with or without expression of the protein-tyrosine phosphatase 1B (PTP1B) and in wild-type and PTP1B-deficient mice chronically treated with APAP. Human primary hepatocytes, Huh7 hepatoma cells with silenced PTP1B, mouse hepatocytes from wild-type and PTP1B-deficient mice, and a mouse model of chronic APAP treatment were used to examine the mechanisms involving PTP1B in the effects of APAP on glucose homeostasis and hepatic insulin signaling. In APAP-treated human hepatocytes at concentrations that did not induce death, phosphorylation of JNK and PTP1B expression and enzymatic activity were increased. APAP pretreatment inhibited activation of the early steps of insulin signaling and decreased Akt phosphorylation. The effects of APAP in insulin signaling were prevented by suramin, a PTP1B inhibitor, or rosiglitazone that decreased PTP1B levels. Likewise, PTP1B deficiency in human or mouse hepatocytes protected against APAP-mediated impairment in insulin signaling. These signaling pathways were modulated in mice with chronic APAP treatment, resulting in protection against APAP-mediated hepatic insulin resistance and alterations in islet alpha/beta cell ratio in PTP1B(-/-) mice. Our results demonstrate negative cross-talk between signaling pathways triggered by APAP and insulin signaling in hepatocytes, which is in part mediated by PTP1B. Moreover, our in vivo data suggest that chronic use of APAP may be associated with insulin resistance in the liver.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.M113.539189

  10 / 4006362 MEDLINE  
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[PMID]: 25187517
[Au] Autor:Li B; Chen P; Qu J; Shi L; Zhuang W; Fu J; Li J; Zhang X; Sun Y; Zhuang W
[Ad] Address:From the Department of Haematology, the Second Affiliated Hospital of Soochow University, Suzhou 215006....
[Ti] Title:Activation of LTBP3 Gene by a Long Noncoding RNA (lncRNA) MALAT1 Transcript in Mesenchymal Stem Cells from Multiple Myeloma.
[So] Source:J Biol Chem;289(42):29365-75, 2014 Oct 17.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Long noncoding RNAs (lncRNAs) are emerging as important regulatory molecules in tumor suppressor and oncogenic pathways. However, the magnitude of the contribution of lncRNA expression to normal human tissues and cancers has not been investigated in a comprehensive manner. Here we explored the biology of the lncRNA MALAT1 and considered the potential significance in mesenchymal stem cells from myeloma patients. By using assays such as RNA interference, luciferase, chromatin immunoprecipitation, and RNA immunoprecipitation, we showed that in mesenchymal stem cells MALAT1 promoted the activation effect of the key transcription factor Sp1 on LTBP3 promoter by modulating recruitment of Sp1 to the LTBP3 gene that regulated the bioavailability of TGF-ß in particular. Our data suggested that lncRNA MALAT1 directly interacted with Sp1 and LTBP3 promoter to increase expression of LTBP3 gene. The specificity and efficiency of activation were ensured by the formation of a stable complex between MALAT1 and the LTBP3 promoter, direct interaction of MALAT1 with Sp1, and recruitment of Sp1 to the promoter. In this study, we showed that the mechanism of transcriptional activation of LTBP3 promoter depended on MALAT1 initiated from neighboring gene LTBP3 and involved both the direct interaction of the Sp1 and promoter-specific activation. Our knowledge of the role of MALAT1 in cellular transformation is pointing toward its potential use as a biomarker and a target for novel therapeutic approaches in multiple myeloma.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.M114.572693


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