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477篇 您的检索式:作者名="Melnick"
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1Mechanisms of action of BCL6 during germinal center B cell development显示文摘The transcriptional repressor B cell lymphoma 6(BCL6) controls a large transcriptional network that is required for the formation and maintenance of germinal centers(GC). GC B cells represent the normal counterpart of most human B-cell lymphomas, which are often characterized by deregulated BCL6 expression or BCL6-mediated pathways. BCL6 suppresses gene transcription largely through recruitment of its co-repressors through its distinct repression domain. Understanding the precise biological roles of each repression domain in normal and malignant B cells is helpful for development of targeted inhibition of BCL6 functions that is emerging as the basis for design of anti-lymphoma therapies. This review focuses on recent progress in the molecular mechanisms of action of BCL6 in B cells and discusses remaining unresolved questions related to how these mechanisms are linked to normal and malignant B cell development.HUANG ChuanXin MELNICK Ari 2015Science China(Life Sciences)2015,58,12:3
2Central role of myeloid MCPIP1 in protecting against LPSinduced inflammation and lung injury显示文摘Although systemic inflammatory responses attributable to infection may lead to significant lung injury,the precise molecular mechanisms leading to lung damage are poorly understood and therapeutic options remain limited.Here,we show that myeloid monocyte chemotactic protein-inducible protein 1(MCPIP1)plays a central role in protecting against LPS-induced inflammation and lung injury.Myeloid-specific MCPIP1 knockout mice developed spontaneous inflammatory syndromes,but at a late age compared to global MCPIP1 knockout mice.Moreover,mice with a myeloid-specific deletion of MCPIP1 were extremely sensitive to LPS-induced lung injury due to overproduction of proinflammatory cytokines and chemokines.We identified C/EBPβand C/EBPδ,two critical transcriptional factors that drive cytokine production and lung injury,as targets of MCPIP1 RNase.LPS administration caused MCPIP1 protein degradation in the lungs.Pharmacological inhibition of MALT1,a paracaspase that cleaves MCPIP1,by MI-2 selectively increased the MCPIP1 protein levels in macrophages and in the lungs.Meanwhile,administration of MI-2 protected mice from LPS-induced inflammation,lung injury and death.Collectively,these results indicate that myeloid MCPIP1 is central in controlling LPS-induced inflammation and lung injury.Pharmacological inhibition of MALT1 protease activity may be a good strategy to treat inflammatory diseases by enhancing MCPIP1 expression in myeloid cells.Yong Li Xuan Huang Shengping Huang Hui He Tianhua Lei Fatma Saaoud Xiao-Qiang Yu Ari Melnick Anil Kumar Christopher J Papasian Daping Fan Mingui Fu 2017Signal Transduction and Targeted Therapy2017,2,1:2
3Deconstructing a disease:RARalpha, its fusion partners, and their roles in the pathogenesis of acute promyelocytic leukemia显示文摘Melnick A Licht JD 1999Blood1999,93,10:1
4Urolithiasis and bladder carcinogenicity of melamine in rodents 显示文摘Melnick RL Boorman GA Haseman JK 1984Toxicol Appl Pharmacol1984,72,:1
5Enterovirus type 71 infections:a varied clinical pattern sometimes mimicking paralytic poliomyelitis显示文摘 1984Rev Infect Dis1984,62,:1
6Deconstructing a disease: RARalpha, its fusion partners, and their roles in the pathogenesis of acute promyelocytic leukemia显示文摘Melnick A Licht JD 1999Blood1999,93,:1
7Vascular calcification in chronic kidney failure: Role of vitamin D receptor 显示文摘WU-WONG J R MELNICK J 2007Curr Opin Investig Drugs2007,8,3:1
8Delayed side effects of droperidol after ambulatory general anesthesia显示文摘Melnick B Sawyer R Karambelkar D 0,,:1
9BCL6 repression of EP300 in human diffuse large B cell lymphoma cells provides a basis for rational combinatorial therapy显示文摘Cerchietti Leandro C Hatzi Katerina Caldas-Lopes Eloisi Yang Shao Ning Figueroa Maria E Morin Ryan D Hirst Martin Mendez Lourdes Shaknovich Rita Cole Philip A Bhalla Kapil Gascoyne Randy D Marra Marco Chiosis Gabriela Melnick Ari 2010Journal of Clinical Investigation2010,,12:1
10Urolithiasis and bladder carcinogenicity of melamine ill rodents 显示文摘Melnick RL Boorman GA Haseman JK 1984Toxicol Appi Pharmacol1984,72,:1
11Cytomegalovirus infection andatherosclerosis显示文摘Adam E Melnick JL DeBakey ME 1997Cent Eur J Public Health1997,5,:1
12Dentin dysplasia type 1: a scanning electron microscopic analysis of the primary dentition 显示文摘Melnick M Levin L Brady J 1980Oral Surg1980,50,7:1
13Develop- mental neurotoxicity of perfluorinated chemicals modeled in vitro显示文摘Slotkin TA MacKillop EA Melnick RL 2008Environ Health Perspect2008,116,6:1
14Expression of apoptosis, cell proliferation, and drug resistance genes in pediatric Wilms'tumors显示文摘Ramachandran C Melnick S J Escalon E 2000Anticancer Res2000,20,5:1
15Vascular calcification in chronic kidney failure: Role of vitamin D receptor 显示文摘WU-WONG J R MELNICK J 2007Curt Opin Investig Drugs2007,8,:1
16Computer-based testing in assessment of physician competence显示文摘Melnick D 1988Issues1988,9,1:1
17Comparison of six clinically used external defibrillators in swine 显示文摘Walker R G Melnick S B Chapman F W 2003Resuscitation2003,57,1:1
18Identification of NVP-TAE684,a potent,selective,and efficacious inhibitor of NVP-TAE684,a potent,selective,and efficacious inhibitor of NPM-ALK显示文摘Galkin AV Melnick JS Kim S 2007Proc Natl Acad Sci USA2007,104,:1
19Summary of the national toxicology program's report of the endocrine disruptors low-dose peer review显示文摘Melnick R Lucier G Wolfe M 0,,04:1
20Urolithiasis and bladder carcinogenicity of melamine in rodents显示文摘Melnick RL Boorman GA Haseman JK 1984Toxicol Appl Pharmacol1984,72,2:1
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