Ricardo Weinlich

@einstein.br

Senior Leader Research. Institute of Education and Research.
Hospital Israelita Albert Einstein

Ricardo Weinlich


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https://researchid.co/rweinlich

RESEARCH, TEACHING, or OTHER INTERESTS

Molecular Biology, Immunology and Allergy, Immunology
48

Scopus Publications

10991

Scholar Citations

28

Scholar h-index

37

Scholar i10-index

Scopus Publications

  • Unraveling Zika virus-induced cell death pathways in eradicating embryonal central nervous system tumors
    Rafaela Rosa-Ribeiro, Mateus Lucas Falco, Janaina Sena de Souza, Oswaldo Keith Okamoto, Ricardo Weinlich
    Neuroscience, 2025
  • An Extended Flow Cytometry Evaluation of ex Vivo Expanded NK Cells Using K562.Clone1, a Feeder Cell Line Manufactured in Brazil
    Caroline Mitiká Watanabe, Caroline Ishihama Suzuki, Alessandro Marins dos Santos, Thiago Pinheiro Arrais Aloia, Grace Lee, David Wald, Oswaldo Keith Okamoto, Julia T. Cottas de Azevedo, Juliana Aparecida Preto de Godoy, Fabio P.S. Santos, Ricardo Weinlich, Lucila N. Kerbauy, Jose Mauro Kutner, Raquel de Melo Alves Paiva, Nelson Hamerschlak
    Transplantation and Cellular Therapy, 2024
  • Inflammatory pathways and anti-inflammatory therapies in sickle cell disease
    Karina Tozatto‐Maio, Felipe A. Rós, Ricardo Weinlich, Vanderson Rocha
    Hemasphere, 2024
    Sickle cell disease (SCD) is a monogenic disease, resulting from a single‐point mutation, that presents a complex pathophysiology and high clinical heterogeneity. Inflammation stands as a prominent characteristic of SCD. Over the past few decades, the role of different cells and molecules in the regulation of the inflammatory process has been elucidated. In conjunction with the polymerization of hemoglobin S (HbS), intravascular hemolysis, which releases free heme, HbS, and hemoglobin‐related damage‐associated molecular patterns, initiates multiple inflammatory pathways that are not yet fully comprehended. These complex phenomena lead to a vicious cycle that perpetuates vaso‐occlusion, hemolysis, and inflammation. To date, few inflammatory biomarkers can predict disease complications; conversely, there is a plethora of therapies that reduce inflammation in SCD, although clinical outcomes vary widely. Importantly, whether the clinical heterogeneity and complications are related to the degree of inflammation is not known. This review aims to further our understanding of the roles of main immune cells, and other inflammatory factors, as potential prognostic biomarkers for predicting clinical outcomes or identifying novel treatments for SCD.
  • The interaction between RIPK1 and FADD controls perinatal lethality and inflammation
    Diego A. Rodriguez, Bart Tummers, Jeremy J.P. Shaw, Giovanni Quarato, Ricardo Weinlich, James Cripps, Patrick Fitzgerald, Laura J. Janke, Stephane Pelletier, Jeremy Chase Crawford, Douglas R. Green
    Cell Reports, 2024
    Perturbation of the apoptosis and necroptosis pathways critically influences embryogenesis. Receptor-associated protein kinase-1 (RIPK1) interacts with Fas-associated via death domain (FADD)-caspase-8-cellular Flice-like inhibitory protein long (cFLIP L ) to regulate both extrinsic apoptosis and necroptosis. Here, we describe Ripk1 -mutant animals ( Ripk1 R588E [RE]) in which the interaction between FADD and RIPK1 is disrupted, leading to embryonic lethality. This lethality is not prevented by further removal of the kinase activity of Ripk1 ( Ripk1 R588E K45A [REKA]). Both Ripk1 RE and Ripk1 REKA animals survive to adulthood upon ablation of Ripk3 . While embryonic lethality of Ripk1 RE mice is prevented by ablation of the necroptosis effector mixed lineage kinase-like (MLKL), animals succumb to inflammation after birth. In contrast, Mlkl ablation does not prevent the death of Ripk1 REKA embryos, but animals reach adulthood when both MLKL and caspase-8 are removed. Ablation of the nucleic acid sensor Zbp1 largely prevents lethality in both Ripk1 RE and Ripk1 REKA embryos. Thus, the RIPK1-FADD interaction prevents Z-DNA binding protein-1 (ZBP1)-induced, RIPK3-caspase-8-mediated embryonic lethality, affected by the kinase activity of RIPK1.
  • Mature tertiary lymphoid structures are key niches of tumour-specific immune responses in pancreatic ductal adenocarcinomas
    Gabriela Sarti Kinker, Glauco Akelinghton Freire Vitiello, Ariane Barros Diniz, Mariela Pires Cabral-Piccin, Pedro Henrique Barbosa Pereira, Maria Letícia Rodrigues Carvalho, Wallax Augusto Silva Ferreira, Alexandre Silva Chaves, Amanda Rondinelli, Arianne Fagotti Gusmão, Alexandre Defelicibus, Gabriel Oliveira dos Santos, Warley Abreu Nunes, Laura Carolina López Claro, Talita Magalhães Bernardo, Ricardo Tadashi Nishio, Adhemar Monteiro Pacheco, Ana Carolina Laus, Lidia Maria Rebolho Batista Arantes, Julia Lima Fleck, Victor Hugo Fonseca de Jesus, André de Moricz, Ricardo Weinlich, Felipe José Fernandez Coimbra, Vladmir Cláudio Cordeiro de Lima, Tiago da Silva Medina
    Gut, 2023
    ObjectiveTo better understand the immune microenvironment of pancreatic ductal adenocarcinomas (PDACs), here we explored the relevance of T and B cell compartmentalisation into tertiary lymphoid structures (TLSs) for the generation of local antitumour immunity.DesignWe characterised the functional states and spatial organisation of PDAC-infiltrating T and B cells using single-cell RNA sequencing (scRNA-seq), flow cytometry, multicolour immunofluorescence, gene expression profiling of microdissected TLSs, as well as in vitro assays. In addition, we performed a pan-cancer analysis of tumour-infiltrating T cells using scRNA-seq and sc T cell receptor sequencing datasets from eight cancer types. To evaluate the clinical relevance of our findings, we used PDAC bulk RNA-seq data from The Cancer Genome Atlas and the PRINCE chemoimmunotherapy trial.ResultsWe found that a subset of PDACs harbours fully developed TLSs where B cells proliferate and differentiate into plasma cells. These mature TLSs also support T cell activity and are enriched with tumour-reactive T cells. Importantly, we showed that chronically activated, tumour-reactive T cells exposed to fibroblast-derived TGF-β may act as TLS organisers by producing the B cell chemoattractant CXCL13. Identification of highly similar subsets of clonally expandedCXCL13+tumour-infiltrating T cells across multiple cancer types further indicated a conserved link between tumour-antigen recognition and the allocation of B cells within sheltered hubs in the tumour microenvironment. Finally, we showed that the expression of a gene signature reflecting mature TLSs was enriched in pretreatment biopsies from PDAC patients with longer survival after receiving different chemoimmunotherapy regimens.ConclusionWe provided a framework for understanding the biological role of PDAC-associated TLSs and revealed their potential to guide the selection of patients for future immunotherapy trials.
  • Higher Mixed lineage Kinase Domain-like protein (MLKL) is associated with worst overall survival in adult-type diffuse glioma patients
    Guilherme Afonso Vergara, Gisele Cristine Eugenio, Suzana Maria Fleury Malheiros, Elivane da Silva Victor, Ricardo Weinlich
    Plos One, 2023
    Introduction Recently, the search for novel molecular markers in adult-type diffuse gliomas has grown substantially, yet with few novel breakthroughs. As the presence of a necrotic center is a differential diagnosis for more aggressive entities, we hypothesized that genes involved in necroptosis may play a role in tumor progression. Aim Given that MLKL is the executioner of the necroptotic pathway, we evaluated whether this gene would help to predict prognosis of adult gliomas patients. Methods We analyzed a publicly available retrospective cohort (n = 530) with Kaplan Meier survival analysis (p<0.0001) and both uni- and multivariate Cox regression models. Results We determined that MLKL is an independent predictive prognostic marker for overall survival in these patients (HR: 2.56, p<0.001), even when controlled by the CNS5 gold-standard markers, namely IDH mutation and 1p/19q Codeletion (HR: 1.68, p = 0.013). These findings were confirmed in a validation cohort (n = 325), using the same cutoff value. Interestingly, higher expression of MLKL is associated with worse clinical outcome for adult-type diffuse glioma patients, which is opposite to what was found in other cell cancer types, suggesting that necroptosis undertakes an atypical detrimental role in glioma progression.
  • Ex vivo gene therapy for lysosomal storage disorders: future perspectives
    Edina Poletto, Andrew Oliveira Silva, Ricardo Weinlich, Priscila Keiko Matsumoto Martin, Davi Coe Torres, Roberto Giugliani, Guilherme Baldo
    Expert Opinion on Biological Therapy, 2023
    Introduction Lysosomal storage disorders (LSD) are a group of monogenic rare diseases caused by pathogenic variants in genes that encode proteins related to lysosomal function. These disorders are good candidates for gene therapy for different reasons: they are monogenic, most of lysosomal proteins are enzymes that can be secreted and cross-correct neighboring cells, and small quantities of these proteins are able to produce clinical benefits in many cases. Ex vivo gene therapy allows for autologous transplant of modified cells from different sources, including stem cells and hematopoietic precursors. Areas covered Here, we summarize the main gene therapy and genome editing strategies that are currently being used as ex vivo gene therapy approaches for lysosomal disorders, highlighting important characteristics, such as vectors used, strategies, types of cells that are modified and main results in different disorders. Expert opinion Clinical trials are already ongoing, and soon approved therapies for LSD based on ex vivo gene therapy approaches should reach the market.
  • TNF-mediated alveolar macrophage necroptosis drives disease pathogenesis during respiratory syncytial virus infection
    Leonardo Duarte Santos, Krist Helen Antunes, Stéfanie Primon Muraro, Gabriela Fabiano de Souza, Amanda Gonzalez da Silva, Jaqueline de Souza Felipe, Larissa Cardoso Zanetti, Rafael Sanguinetti Czepielewski, Karen Magnus, Marcelo Scotta, Rita Mattiello, Fabio Maito, Ana Paula Duarte de Souza, Ricardo Weinlich, Marco Aurélio Ramirez Vinolo, Bárbara Nery Porto
    European Respiratory Journal, 2021
    Respiratory syncytial virus (RSV) is the major cause of acute bronchiolitis in infants under 2 years old. Necroptosis has been implicated in the outcomes of respiratory virus infections. We report that RSV infection triggers necroptosis in primary mouse macrophages and human monocytes in a RIPK1-, RIPK3- and MLKL-dependent manner. Moreover, necroptosis pathways are harmful to RSV clearance from alveolar macrophages. Additionally,Ripk3−/−mice were protected from RSV-induced weight loss and presented with reduced viral loads in the lungs.Alveolar macrophage depletion also protected mice from weight loss and decreased lung RSV virus load. Importantly, alveolar macrophage depletion abolished the upregulation ofRipk3andMlklgene expression induced by RSV infection in the lung tissue.Autocrine tumor necrosis factor (TNF)-mediated RSV-triggered macrophage necroptosis and necroptosis pathways were also involved in TNF secretion even when macrophages were committed to cell death, which can worsen lung injury during RSV infection. In line,Tnfr1−/−mice had a marked decrease inRipk3andMlklgene expression and a sharp reduction in the numbers of necrotic alveolar macrophages in the lungs. Finally, we provide evidence that elevated nasal levels of TNF are associated with disease severity in infants with RSV bronchiolitis.We propose that targeting TNF and/or the necroptotic machinery may be valuable therapeutic approaches to reduce the respiratory morbidity caused by RSV infection in young children.
  • Necroptosis, the Other Main Caspase-Independent Cell Death
    Larissa C. Zanetti, Ricardo Weinlich
    Advances in Experimental Medicine and Biology, 2021
  • Lapachol acetylglycosylation enhances its cytotoxic and pro-apoptotic activities in HL60 cells
    Lucas Bonfim Marques, Flaviano Melo Ottoni, Mauro Cunha Xavier Pinto, Juliana Martins Ribeiro, Fernanda S. de Sousa, Ricardo Weinlich, Nathalia Cruz de Victo, Jaffar Kisitu, Anna-Katharina Holzer, Marcel Leist, Ricardo José Alves, Elaine Maria Souza-Fagundes
    Toxicology in Vitro, 2020
  • RIPK3 is a novel prognostic marker for lower grade glioma and further enriches IDH mutational status subgrouping
    Guilherme Afonso Vergara, Gisele Cristine Eugenio, Suzana Maria Fleury Malheiros, Elivane da Silva Victor, Ricardo Weinlich
    Journal of Neuro Oncology, 2020
  • Comparison of 2D and 3D cell culture models for cell growth, gene expression and drug resistance
    Julia C. Fontoura, Christian Viezzer, Fabiana G. dos Santos, Rosane A. Ligabue, Ricardo Weinlich, Renato D. Puga, Dyeison Antonow, Patricia Severino, Cristina Bonorino
    Materials Science and Engineering C, 2020
  • Frontline Science: Autophagy is a cell autonomous effector mechanism mediated by NLRP3 to control Trypanosoma cruzi infection
    Kely C Matteucci, Gustavo J S Pereira, Ricardo Weinlich, Karina R Bortoluci
    Journal of Leukocyte Biology, 2019
  • The impairment in the NLRP3-induced NO secretion renders astrocytes highly permissive to T. cruzi replication
    Aline L Pacheco, Gabriella Vicentini, Kely C Matteucci, Rafaela Rosa Ribeiro, Ricardo Weinlich, Karina R Bortoluci
    Journal of Leukocyte Biology, 2019
  • Pattern recognition receptors and the host cell death molecular machinery
    Gustavo P. Amarante-Mendes, Sandy Adjemian, Laura Migliari Branco, Larissa C. Zanetti, Ricardo Weinlich, Karina R. Bortoluci
    Frontiers in Immunology, 2018
  • A Dual Role of Caspase-8 in Triggering and Sensing Proliferation-Associated DNA Damage, a Key Determinant of Liver Cancer Development
    Yannick Boege, Mohsen Malehmir, Marc E. Healy, Kira Bettermann, Anna Lorentzen, Mihael Vucur, Akshay K. Ahuja, Friederike Böhm, Joachim C. Mertens, Yutaka Shimizu, Lukas Frick, Caroline Remouchamps, Karun Mutreja, Thilo Kähne, Devakumar Sundaravinayagam, Monika J. Wolf, Hubert Rehrauer, Christiane Koppe, Tobias Speicher, Susagna Padrissa-Altés, Renaud Maire, Jörn M. Schattenberg, Ju-Seong Jeong, Lei Liu, Stefan Zwirner, Regina Boger, Norbert Hüser, Roger J. Davis, Beat Müllhaupt, Holger Moch, Henning Schulze-Bergkamen, Pierre-Alain Clavien, Sabine Werner, Lubor Borsig, Sanjiv A. Luther, Philipp J. Jost, Ricardo Weinlich, Kristian Unger, Axel Behrens, Laura Hillert, Christopher Dillon, Michela Di Virgilio, David Wallach, Emmanuel Dejardin, Lars Zender, Michael Naumann, Henning Walczak, Douglas R. Green, Massimo Lopes, Inna Lavrik, Tom Luedde, Mathias Heikenwalder, Achim Weber
    Cancer Cell, 2017
  • Necroptosis in development, inflammation and disease
    Ricardo Weinlich, Andrew Oberst, Helen M. Beere, Douglas R. Green
    Nature Reviews Molecular Cell Biology, 2017
  • Characterization of RIPK3-mediated phosphorylation of the activation loop of MLKL during necroptosis
    D A Rodriguez, R Weinlich, S Brown, C Guy, P Fitzgerald, C P Dillon, A Oberst, G Quarato, J Low, J G Cripps, T Chen, D R Green
    Cell Death and Differentiation, 2016
  • Myeloid-derived suppressor activity is mediated by monocytic lineages maintained by continuous inhibition of extrinsic and intrinsic death pathways
    Jessica M. Haverkamp, Amber M. Smith, Ricardo Weinlich, Christopher P. Dillon, Joseph E. Qualls, Geoffrey Neale, Brian Koss, Young Kim, Vincenzo Bronte, Marco J. Herold, Douglas R. Green, Joseph T. Opferman, Peter J. Murray
    Immunity, 2014
  • Synchronized renal tubular cell death involves ferroptosis
    Andreas Linkermann, Rachid Skouta, Nina Himmerkus, Shrikant R. Mulay, Christin Dewitz, Federica De Zen, Agnes Prokai, Gabriele Zuchtriegel, Fritz Krombach, Patrick-Simon Welz, Ricardo Weinlich, Tom Vanden Berghe, Peter Vandenabeele, Manolis Pasparakis, Markus Bleich, Joel M. Weinberg, Christoph A. Reichel, Jan Hinrich Bräsen, Ulrich Kunzendorf, Hans-Joachim Anders, Brent R. Stockwell, Douglas R. Green, Stefan Krautwald
    Proceedings of the National Academy of Sciences of the United States of America, 2014
  • The Two Faces of Receptor Interacting Protein Kinase-1
    Ricardo Weinlich, Douglas R. Green
    Molecular Cell, 2014
  • RIPK1 blocks early postnatal lethality mediated by caspase-8 and RIPK3
    Christopher P. Dillon, Ricardo Weinlich, Diego A. Rodriguez, James G. Cripps, Giovanni Quarato, Prajwal Gurung, Katherine C. Verbist, Taylor L. Brewer, Fabien Llambi, Yi-Nan Gong, Laura J. Janke, Michelle A. Kelliher, Thirumala-Devi Kanneganti, Douglas R. Green
    Cell, 2014
  • FADD and caspase-8 mediate priming and activation of the canonical and noncanonical Nlrp3 inflammasomes
    Prajwal Gurung, Paras K Anand, R K Subbarao Malireddi, Lieselotte Vande Walle, Nina Van Opdenbosch, Christopher P Dillon, Ricardo Weinlich, Douglas R Green, Mohamed Lamkanfi, Thirumala-Devi Kanneganti
    Journal of Immunology, 2014
  • A novel cytotoxic sequence contributes to influenza a viral protein PB1-F2 pathogenicity and predisposition to secondary bacterial infection
    Irina V. Alymova, Amali Samarasinghe, Peter Vogel, Amanda M. Green, Ricardo Weinlich, Jonathan A. McCullers
    Journal of Virology, 2014
  • Erratum: C11orf95-RELA fusions drive oncogenic NF-ΰ B signalling in ependymoma (Nature (2014) 506 (451-455 ) DOI:10.1038/nature13109)
    Matthew Parker, Kumarasamypet M. Mohankumar, Chandanamali Punchihewa, Ricardo Weinlich, James D. Dalton, Yongjin Li, Ryan Lee, Ruth G. Tatevossian, Timothy N. Phoenix, Radhika Thiruvenkatam, Elsie White, Bo Tang, Wilda Orisme, Kirti Gupta, Michael Rusch, Xiang Chen, Yuxin Li, Panduka Nagahawhatte, Erin Hedlund, David Finkelstein, Gang Wu, Sheila Shurtleff, John Easton, Kristy Boggs, Donald Yergeau, Bhavin Vadodaria, Heather L. Mulder, Jared Becksfort, Pankaj Gupta, Robert Huether, Jing Ma, Guangchun Song, Amar Gajjar, Thomas Merchant, Frederick Boop, Amy A. Smith, Li Ding, Charles Lu, Kerri Ochoa, David Zhao, Robert S. Fulton, Lucinda L. Fulton, Elaine R. Mardis, Richard K. Wilson, James R. Downing, Douglas R. Green, Jinghui Zhang, David W. Ellison, Richard J. Gilbertson
    Nature, 2014
  • C11orf95-RELA fusions drive oncogenic NF-κB signalling in ependymoma
    Matthew Parker, Kumarasamypet M. Mohankumar, Chandanamali Punchihewa, Ricardo Weinlich, James D. Dalton, Yongjin Li, Ryan Lee, Ruth G. Tatevossian, Timothy N. Phoenix, Radhika Thiruvenkatam, Elsie White, Bo Tang, Wilda Orisme, Kirti Gupta, Michael Rusch, Xiang Chen, Yuxin Li, Panduka Nagahawhatte, Erin Hedlund, David Finkelstein, Gang Wu, Sheila Shurtleff, John Easton, Kristy Boggs, Donald Yergeau, Bhavin Vadodaria, Heather L. Mulder, Jared Becksfort, Pankaj Gupta, Robert Huether, Jing Ma, Guangchun Song, Amar Gajjar, Thomas Merchant, Frederick Boop, Amy A. Smith, Li Ding, Charles Lu, Kerri Ochoa, David Zhao, Robert S. Fulton, Lucinda L. Fulton, Elaine R. Mardis, Richard K. Wilson, James R. Downing, Douglas R. Green, Jinghui Zhang, David W. Ellison, Richard J. Gilbertson
    Nature, 2014
  • Protective Roles for Caspase-8 and cFLIP in Adult Homeostasis
    Ricardo Weinlich, Andrew Oberst, Christopher P. Dillon, Laura J. Janke, Sandra Milasta, John R. Lukens, Diego A. Rodriguez, Prajwal Gurung, Chandra Savage, Thirumala D. Kanneganti, Douglas R. Green
    Cell Reports, 2013
  • Two independent pathways of regulated necrosis mediate ischemia-reperfusion injury
    Andreas Linkermann, Jan Hinrich Bräsen, Maurice Darding, Mi Kyung Jin, Ana B. Sanz, Jan-Ole Heller, Federica De Zen, Ricardo Weinlich, Alberto Ortiz, Henning Walczak, Joel M. Weinberg, Douglas R. Green, Ulrich Kunzendorf, Stefan Krautwald
    Proceedings of the National Academy of Sciences of the United States of America, 2013
  • Survival Function of the FADD-CASPASE-8-cFLIPL Complex
    Christopher P. Dillon, Andrew Oberst, Ricardo Weinlich, Laura J. Janke, Tae-Bong Kang, Tehila Ben-Moshe, Tak W. Mak, David Wallach, Douglas R. Green
    Cell Reports, 2012
  • Dichotomy between RIP1- and RIP3-mediated necroptosis in tumor necrosis factor-α-induced shock
    Andreas Linkermann, Jan H. Bräsen, Federica De Zen, Ricardo Weinlich, Reto A. Schwendener, Douglas R. Green, Ulrich Kunzendorf, Stefan Krautwald
    Molecular Medicine, 2012
  • Ripped to death
    Ricardo Weinlich, Christopher P. Dillon, Douglas R. Green
    Trends in Cell Biology, 2011
  • RIPK-dependent necrosis and its regulation by caspases: A mystery in five acts
    Douglas R. Green, Andrew Oberst, Christopher P. Dillon, Ricardo Weinlich, Guy S. Salvesen
    Molecular Cell, 2011
  • Scientists contemplate unexplained death in Austrian Alps
    Charles Miller, Christopher Dillon, Jennifer Martinez, Melissa Parsons, Ricardo Weinlich, Gerry Melino
    EMBO Molecular Medicine, 2011
  • Catalytic activity of the caspase-8-FLIP L complex inhibits RIPK3-dependent necrosis
    Andrew Oberst, Christopher P. Dillon, Ricardo Weinlich, Laura L. McCormick, Patrick Fitzgerald, Cristina Pop, Razq Hakem, Guy S. Salvesen, Douglas R. Green
    Nature, 2011
  • Hypoxia inducible factor-dependent regulation of angiogenesis by nitro-fatty acids
    Martina Rudnicki, Luciane A. Faine, Nathalie Dehne, Dmitry Namgaladze, Simone Ferderbar, Ricardo Weinlich, Gustavo P. Amarante-Mendes, Chao Y.I. Yan, José E. Krieger, Bernhard Brüne, Dulcineia S.P. Abdalla
    Arteriosclerosis Thrombosis and Vascular Biology, 2011
  • Control of death receptor ligand activity by posttranslational modifications
    R. Weinlich, T. Brunner, G. P. Amarante-Mendes
    Cellular and Molecular Life Sciences, 2010
  • Melatonin protects CD4+ T cells from activation-induced cell death by blocking NFAT-mediated CD95 ligand upregulation
    Alziana Moreno da Cunha Pedrosa, Ricardo Weinlich, Giuliana Patricia Mognol, Bruno Kaufmann Robbs, João Paulo de Biaso Viola, Ana Campa, Gustavo Pessini Amarante-Mendes
    Journal of Immunology, 2010
  • TLR4/MYD88-dependent, LPS-induced synthesis of PGE2 by macrophages or dendritic cells prevents anti-CD3-mediated CD95L upregulation in T cells
    R Weinlich, K R Bortoluci, C F Chehab, C H Serezani, A G Ulbrich, M Peters-Golden, M Russo, G P Amarante-Mendes
    Cell Death and Differentiation, 2008
  • An oligonucleotide primer set for PCR amplification of the complete honey bee mitochondrial genome
    Maria Cristina Arias, Daniela Silvestre, Flávio de Oliveira Francisco, Ricardo Weinlich, Walter Steven Sheppard
    Apidologie, 2008
  • Sustained activation of p53 in confluent nucleotide excision repair-deficient cells resistant to ultraviolet-induced apoptosis
    Helotonio Carvalho, Tatiana G. Ortolan, Tomás dePaula, Ricardo A. Leite, Ricardo Weinlich, Gustavo P. Amarante-Mendes, Carlos Frederico Martins Menck
    DNA Repair, 2008
  • BnP1, a novel P-I metalloproteinase from Bothrops neuwiedi venom: Biological effects benchmarking relatively to jararhagin, a P-III SVMP
    C. Baldo, I. Tanjoni, I.R. León, I.F.C. Batista, M.S. Della-Casa, P.B. Clissa, R. Weinlich, M. Lopes-Ferreira, I. Lebrun, G.P. Amarante-Mendes, V.M. Rodrigues, J. Perales, R.H. Valente, A.M. Moura-da-Silva
    Toxicon, 2008
  • Pomolic acid may overcome multidrug resistance mediated by overexpression of anti-apoptotic Bcl-2 proteins
    Janaina Fernandes, Ricardo Weinlich, Rachel Oliveira Castilho, Gustavo Pessini Amarante-Mendes, Cerli Rocha Gattass
    Cancer Letters, 2007
  • Jararhagin, a snake venom metalloproteinase, induces a specialized form of apoptosis (anoikis) selective to endothelial cells
    I. Tanjoni, R. Weinlich, M. S. Della-Casa, P. B. Clissa, R. F. Saldanha-Gama, M. S. de Freitas, C. Barja-Fidalgo, G. P. Amarante-Mendes, A. M. Moura-da-Silva
    Apoptosis, 2005
  • Pomolic acid triggers mitochondria-dependent apoptotic cell death in leukemia cell line
    J FERNANDES, R WEINLICH, R OLIVEIRACASTILHO, M COELHOKAPLAN, G AMARANTEMENDES, C GATTASS
    Cancer Letters, 2005
  • Mitochondrial DNA restriction and genomic maps of seven species of Melipona (Apidae: Meliponini)
    Ricardo Weinlich, Fl�vio de Oliveira Francisco, Maria Cristina Arias
    Apidologie, 2004
  • Comparison of the anti-apoptotic effects of Bcr-Abl, Bcl-2 and Bcl-xL following diverse apoptogenic stimuli
    Gabriela Brumatti, Ricardo Weinlich, Cristina F Chehab, Monica Yon, Gustavo P Amarante-Mendes
    FEBS Letters, 2003
  • Effect of cell confluence on ultraviolet light apoptotic responses in DNA repair deficient cells
    Helotonio Carvalho, Renata Maria Augusto da Costa, Vanessa Chiganças, Ricardo Weinlich, Gabriela Brumatti, Gustavo P. Amarante-Mendes, Alain Sarasin, Carlos Frederico Martins Menck
    Mutation Research Reviews in Mutation Research, 2003
  • A scientific note on mtDNA gene order rearrangements among highly eusocial bees (Hymenoptera, Apidae)
    Daniela Silvestre, Fl�vio de Oliveira Francisco, Ricardo Weinlich, Maria Cristina Arias
    Apidologie, 2002

RECENT SCHOLAR PUBLICATIONS

  • Lapachol acetylglycosylation enhances its cytotoxic and pro-apoptotic activities in HL60 cells
    LB Marques, FM Ottoni, MCX Pinto, JM Ribeiro, FS de Sousa, R Weinlich, ...
    Toxicology in Vitro 65, 104772 , 2020
    2020
    Citations: 22
  • RIPK3 is a novel prognostic marker for lower grade glioma and further enriches IDH mutational status subgrouping
    GA Vergara, GC Eugenio, SMF Malheiros, ES Victor, R Weinlich
    Journal of Neuro-Oncology 147 (3), 587-594 , 2020
    2020
    Citations: 28
  • Comparison of 2D and 3D cell culture models for cell growth, gene expression and drug resistance
    JC Fontoura, C Viezzer, FG dos Santos, RA Ligabue, R Weinlich, ...
    Materials Science and Engineering: C 107, 110264 , 2020
    2020
    Citations: 478
  • Frontline Science: Autophagy is a cell autonomous effector mechanism mediated by NLRP3 to control Trypanosoma cruzi infection
    KC Matteucci, GJS Pereira, R Weinlich, KR Bortoluci
    Journal of leukocyte biology 106 (3), 531-540 , 2019
    2019
    Citations: 23
  • The impairment in the NLRP3‐induced NO secretion renders astrocytes highly permissive to T. cruzi replication
    AL Pacheco, G Vicentini, KC Matteucci, RR Ribeiro, R Weinlich, ...
    Journal of Leukocyte Biology 106 (1), 201-207 , 2019
    2019
    Citations: 20
  • Pattern recognition receptors and the host cell death molecular machinery
    GP Amarante-Mendes, S Adjemian, LM Branco, LC Zanetti, R Weinlich, ...
    Frontiers in immunology 9, 2379 , 2018
    2018
    Citations: 1044
  • A dual role of caspase-8 in triggering and sensing proliferation-associated DNA damage, a key determinant of liver cancer development
    Y Boege, M Malehmir, ME Healy, K Bettermann, A Lorentzen, M Vucur, ...
    Cancer Cell 32 (3), 342-359. e10 , 2017
    2017
    Citations: 181
  • Necroptosis in development, inflammation and disease
    R Weinlich, A Oberst, HM Beere, DR Green
    Nature reviews Molecular cell biology 18 (2), 127-136 , 2017
    2017
    Citations: 1121
  • Characterization of RIPK3-mediated phosphorylation of the activation loop of MLKL during necroptosis
    DA Rodriguez, R Weinlich, S Brown, C Guy, P Fitzgerald, CP Dillon, ...
    Cell Death & Differentiation 23 (1), 76-88 , 2016
    2016
    Citations: 437
  • Myeloid-Derived Suppressor Activity Is Mediated by Monocytic Lineages Maintained by Continuous Inhibition of Extrinsic and Intrinsic Death Pathways
    JM Haverkamp, AM Smith, R Weinlich, CP Dillon, JE Qualls, G Neale, ...
    Immunity 41 (6), 947-959 , 2014
    2014
    Citations: 189
  • Synchronized renal tubular cell death involves ferroptosis
    A Linkermann, R Skouta, N Himmerkus, SR Mulay, C Dewitz, F De Zen, ...
    Proceedings of the National Academy of Sciences 111 (47), 16836-16841 , 2014
    2014
    Citations: 1248
  • The Two Faces of Receptor Interacting Protein Kinase-1
    R Weinlich, DR Green
    Molecular cell 56 (4), 469-480 , 2014
    2014
    Citations: 164
  • RIPK1 blocks early postnatal lethality mediated by caspase-8 and RIPK3
    CP Dillon, R Weinlich, DA Rodriguez, JG Cripps, G Quarato, P Gurung, ...
    Cell 157 (5), 1189-1202 , 2014
    2014
    Citations: 660
  • FADD and caspase-8 mediate priming and activation of the canonical and noncanonical Nlrp3 inflammasomes
    P Gurung, PK Anand, RKS Malireddi, L Vande Walle, N Van Opdenbosch, ...
    The Journal of Immunology 192 (4), 1835-1846 , 2014
    2014
    Citations: 669
  • C11orf95–RELA fusions drive oncogenic NF-κB signalling in ependymoma
    M Parker, KM Mohankumar, C Punchihewa, R Weinlich, JD Dalton, Y Li, ...
    Nature 506 (7489), 451-455 , 2014
    2014
    Citations: 788
  • A novel cytotoxic sequence contributes to influenza A viral protein PB1-F2 pathogenicity and predisposition to secondary bacterial infection
    IV Alymova, A Samarasinghe, P Vogel, AM Green, R Weinlich, ...
    Journal of virology 88 (1), 503-515 , 2014
    2014
    Citations: 66
  • Protective roles for caspase-8 and cFLIP in adult homeostasis
    R Weinlich, A Oberst, CP Dillon, LJ Janke, S Milasta, JR Lukens, ...
    Cell reports 5 (2), 340-348 , 2013
    2013
    Citations: 174
  • Two independent pathways of regulated necrosis mediate ischemia–reperfusion injury
    A Linkermann, JH Bräsen, M Darding, MK Jin, AB Sanz, JO Heller, ...
    Proceedings of the National Academy of Sciences 110 (29), 12024-12029 , 2013
    2013
    Citations: 671
  • Survival function of the FADD-CASPASE-8-cFLIP L complex
    CP Dillon, A Oberst, R Weinlich, LJ Janke, TB Kang, T Ben-Moshe, ...
    Cell reports 1 (5), 401-407 , 2012
    2012
    Citations: 379
  • Dichotomy between RIP1-and RIP3-mediated necroptosis in tumor necrosis factor-α-induced shock
    A Linkermann, JH Bräsen, F De Zen, R Weinlich, RA Schwendener, ...
    Molecular Medicine 18 (4), 577-586 , 2012
    2012
    Citations: 169

MOST CITED SCHOLAR PUBLICATIONS

  • Catalytic activity of the caspase-8-FLIPL complex inhibits RIPK3-dependent necrosis
    A Oberst, CP Dillon, R Weinlich, LL McCormick, P Fitzgerald, C Pop, ...
    Nature 471 (7338), 363-367 , 2011
    2011
    Citations: 1500
  • Synchronized renal tubular cell death involves ferroptosis
    A Linkermann, R Skouta, N Himmerkus, SR Mulay, C Dewitz, F De Zen, ...
    Proceedings of the National Academy of Sciences 111 (47), 16836-16841 , 2014
    2014
    Citations: 1248
  • Necroptosis in development, inflammation and disease
    R Weinlich, A Oberst, HM Beere, DR Green
    Nature reviews Molecular cell biology 18 (2), 127-136 , 2017
    2017
    Citations: 1121
  • Pattern recognition receptors and the host cell death molecular machinery
    GP Amarante-Mendes, S Adjemian, LM Branco, LC Zanetti, R Weinlich, ...
    Frontiers in immunology 9, 2379 , 2018
    2018
    Citations: 1044
  • C11orf95–RELA fusions drive oncogenic NF-κB signalling in ependymoma
    M Parker, KM Mohankumar, C Punchihewa, R Weinlich, JD Dalton, Y Li, ...
    Nature 506 (7489), 451-455 , 2014
    2014
    Citations: 788
  • Two independent pathways of regulated necrosis mediate ischemia–reperfusion injury
    A Linkermann, JH Bräsen, M Darding, MK Jin, AB Sanz, JO Heller, ...
    Proceedings of the National Academy of Sciences 110 (29), 12024-12029 , 2013
    2013
    Citations: 671
  • FADD and caspase-8 mediate priming and activation of the canonical and noncanonical Nlrp3 inflammasomes
    P Gurung, PK Anand, RKS Malireddi, L Vande Walle, N Van Opdenbosch, ...
    The Journal of Immunology 192 (4), 1835-1846 , 2014
    2014
    Citations: 669
  • RIPK1 blocks early postnatal lethality mediated by caspase-8 and RIPK3
    CP Dillon, R Weinlich, DA Rodriguez, JG Cripps, G Quarato, P Gurung, ...
    Cell 157 (5), 1189-1202 , 2014
    2014
    Citations: 660
  • Comparison of 2D and 3D cell culture models for cell growth, gene expression and drug resistance
    JC Fontoura, C Viezzer, FG dos Santos, RA Ligabue, R Weinlich, ...
    Materials Science and Engineering: C 107, 110264 , 2020
    2020
    Citations: 478
  • Characterization of RIPK3-mediated phosphorylation of the activation loop of MLKL during necroptosis
    DA Rodriguez, R Weinlich, S Brown, C Guy, P Fitzgerald, CP Dillon, ...
    Cell Death & Differentiation 23 (1), 76-88 , 2016
    2016
    Citations: 437
  • Survival function of the FADD-CASPASE-8-cFLIP L complex
    CP Dillon, A Oberst, R Weinlich, LJ Janke, TB Kang, T Ben-Moshe, ...
    Cell reports 1 (5), 401-407 , 2012
    2012
    Citations: 379
  • RIPK-dependent necrosis and its regulation by caspases: a mystery in five acts
    DR Green, A Oberst, CP Dillon, R Weinlich, GS Salvesen
    Molecular cell 44 (1), 9-16 , 2011
    2011
    Citations: 206
  • Myeloid-Derived Suppressor Activity Is Mediated by Monocytic Lineages Maintained by Continuous Inhibition of Extrinsic and Intrinsic Death Pathways
    JM Haverkamp, AM Smith, R Weinlich, CP Dillon, JE Qualls, G Neale, ...
    Immunity 41 (6), 947-959 , 2014
    2014
    Citations: 189
  • A dual role of caspase-8 in triggering and sensing proliferation-associated DNA damage, a key determinant of liver cancer development
    Y Boege, M Malehmir, ME Healy, K Bettermann, A Lorentzen, M Vucur, ...
    Cancer Cell 32 (3), 342-359. e10 , 2017
    2017
    Citations: 181
  • Protective roles for caspase-8 and cFLIP in adult homeostasis
    R Weinlich, A Oberst, CP Dillon, LJ Janke, S Milasta, JR Lukens, ...
    Cell reports 5 (2), 340-348 , 2013
    2013
    Citations: 174
  • Dichotomy between RIP1-and RIP3-mediated necroptosis in tumor necrosis factor-α-induced shock
    A Linkermann, JH Bräsen, F De Zen, R Weinlich, RA Schwendener, ...
    Molecular Medicine 18 (4), 577-586 , 2012
    2012
    Citations: 169
  • The Two Faces of Receptor Interacting Protein Kinase-1
    R Weinlich, DR Green
    Molecular cell 56 (4), 469-480 , 2014
    2014
    Citations: 164
  • Jararhagin, a snake venom metalloproteinase, induces a specialized form of apoptosis (anoikis) selective to endothelial cells
    I Tanjoni, R Weinlich, MS Della-Casa, PB Clissa, RF Saldanha-Gama, ...
    Apoptosis 10 (4), 851-861 , 2005
    2005
    Citations: 129
  • Ripped to death
    R Weinlich, CP Dillon, DR Green
    Trends in cell biology 21 (11), 630-637 , 2011
    2011
    Citations: 93
  • BnP1, a novel PI metalloproteinase from Bothrops neuwiedi venom: biological effects benchmarking relatively to jararhagin, a P-III SVMP
    C Baldo, I Tanjoni, IR León, IFC Batista, MS Della-Casa, PB Clissa, ...
    Toxicon 51 (1), 54-65 , 2008
    2008
    Citations: 79