Imperial College London

DrChiaraRecchi

Faculty of MedicineDepartment of Surgery & Cancer

Honorary Senior Lecturer
 
 
 
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c.recchi

 
 
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Location

 

Institute of Reproductive and Developmental BiologyHammersmith Campus

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Summary

 

Publications

Publication Type
Year
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30 results found

Antony J, Zanini E, Birtley JR, Gabra H, Recchi Cet al., 2021, Emerging roles for the GPI-anchored tumor suppressor OPCML in cancers, CANCER GENE THERAPY, Vol: 28, Pages: 18-26, ISSN: 0929-1903

Journal article

Birtley JR, Alomary M, Zanini E, Antony J, Maben Z, Weaver G, von Arx C, Mura M, Marinho AT, Lu H, Morecroft E, Karali E, Chayen N, Tate E, Jurewicz M, Stern L, Recchi C, Gabra Het al., 2019, Inactivating mutations and X-ray crystal structure of the tumor suppressor OPCML reveal cancer-associated functions, Nature Communications, Vol: 10, ISSN: 2041-1723

OPCML, a tumor suppressor gene, is frequently silenced epigenetically in ovarian and other cancers. Here we report, by analysis of databases of tumor sequences, the observation of OPCML somatic missense mutations from various tumor types and the impact of these mutations on OPCML function, by solving the X-ray crystal structure of this glycoprotein to 2.65 Å resolution. OPCML consists of an extended arrangement of three immunoglobulin-like domains and homodimerizes via a network of contacts between membrane-distal domains. We report the generation of a panel of OPCML variants with representative clinical mutations and demonstrate clear phenotypic effects in vitro and in vivo including changes to anchorage-independent growth, interaction with activated cognate receptor tyrosine kinases, cellular migration, invasion in vitro and tumor growth in vivo. Our results suggest that clinically occurring somatic missense mutations in OPCML have the potential to contribute to tumorigenesis in a variety of cancers.

Journal article

Marinho AT, Lu H, Pereira SA, Monteiro E, Gabra H, Recchi Cet al., 2019, Anti-tumorigenic and platinum-sensitizing effects of apolipoprotein A1 and apolipoprotein A1 mimetic peptides in ovarian cancer, Frontiers in Pharmacology, Vol: 9, ISSN: 1663-9812

Objective: Apolipoprotein A1 (ApoA1) is remarkably decreased in serum and ovarian tissues of ovarian cancer patients. ApoA1 and ApoA1 mimetic peptides can sequestrate pro-inflammatory phospholipids, some of which are known to activate a variety of oncogenic pathways. Besides, more intrinsic anti-tumorigenic properties, independent from interaction with lipids, have also been described for ApoA1. We aimed to disclose the effects of ApoA1 and a mimetic peptide on the malignant phenotype of ovarian cancer cells, particularly regarding cell viability, invasiveness and platinum sensitization.Methods: Cells viability was assessed by MTS assay. Extracellular matrix invasion was assessed by transwell and spheroid invasion assays. Western blotting was performed to evaluate the effect of test compounds on intracellular pathways. Sensitization assays were performed in vitro and in the biologically relevant in ovo chorioallantoic membrane model.Results: Both ApoA1 and the mimetic peptide, at a concentration of 100 μg/mL, were able to decrease the viability of SKOV3, CAOV3, and OVCAR3 cells (p < 0.05). The peptide at this concentration was not able to affect the viability of immortalized non-neoplastic ovarian cells (p > 0.05). ApoA1 decreased SKOV3 cells invasiveness at 300 μg/mL after 72 and 96 h of exposure (p < 0.05), while the ApoA1 mimetic peptide prevented cell invasion at 50 and 100 μg/mL (p < 0.01). Treatment with 100 μg/mL of ApoA1 mimetic peptide decreased Akt phosphorylation in SKOV3 cells (p < 0.01). Accordingly, treatment with increasing concentrations of the peptide sensitized SKOV3, OVCAR3 and CAOV3 cells to cisplatin. This synergistic effect was observed both in vitro and in ovo.Conclusions: These results support the role of ApoA1 and ApoA1 mimetics as suppressors of ovarian tumorigenesis and as chemo-sensitising agents.

Journal article

Antony J, Zanini E, Kelly Z, Tan TZ, Karali E, Alomary M, Jung Y, Nixon K, Cunnea P, Fotopoulou C, Paterson A, Roy-Nawathe S, Mills GB, Huang RY-J, Thiery JP, Gabra H, Recchi Cet al., 2018, The tumour suppressor OPCML promotes AXL inactivation by the phosphatase PTPRG in ovarian cancer, EMBO Reports, Vol: 19, ISSN: 1469-221X

In ovarian cancer, the prometastatic RTK AXL promotes motility, invasion and poor prognosis. Here, we show that reduced survival caused by AXL overexpression can be mitigated by the expression of the GPI-anchored tumour suppressor OPCML Further, we demonstrate that AXL directly interacts with OPCML, preferentially so when AXL is activated by its ligand Gas6. As a consequence, AXL accumulates in cholesterol-rich lipid domains, where OPCML resides. Here, phospho-AXL is brought in proximity to the lipid domain-restricted phosphatase PTPRG, which de-phosphorylates the RTK/ligand complex. This prevents AXL-mediated transactivation of other RTKs (cMET and EGFR), thereby inhibiting sustained phospho-ERK signalling, induction of the EMT transcription factor Slug, cell migration and invasion. From a translational perspective, we show that OPCML enhances the effect of the phase II AXL inhibitor R428 in vitro and in vivo We therefore identify a novel mechanism by which two spatially restricted tumour suppressors, OPCML and PTPRG, coordinate to repress AXL-dependent oncogenic signalling.

Journal article

Zhao W, Jamshidiha M, Lanyon-Hogg T, Recchi C, Cota E, Tat EWet al., 2017, Direct targeting of the ras GTPase superfamily through structure-based design, Current Topics in Medicinal Chemistry, Vol: 17, Pages: 16-29, ISSN: 1568-0266

The Ras superfamily of small monomeric GTPases includes some of the most prominent cancer targets for which no selective therapeutic agent has yet been successfully developed. The turn of the millennium saw a resurgence of efforts to target these enzymes using new and improved biophysical techniques to overcome the perceived difficulties of insurmountably high affinity for guanosine nucleotides and flat, flexible topology lacking suitable pockets for small molecule inhibitors. Further, recent investigations have begun to probe the dynamic conformational status of GTP-bound Ras, opening up new mechanisms of inhibition. While much of the literature has focused on the oncogenic Ras proteins, particularly K-Ras, these represent only a small minority of therapeutically interesting targets within the superfamily; for example, the Rab GTPases are the largest subfamily of about 70 members, and present an as yet untapped class of potential targets. The present review documents the key methodologies employed to date in structure-guided attempts to drug the Ras GTPases, and forecasts their transferability to other similarly challenging proteins in the superfamily.

Journal article

Zanini E, Louis LS, Antony J, Karali E, Okon IS, McKie AB, Vaughan S, El-Bahrawy M, Stebbing J, Recchi C, Gabra Het al., 2017, The tumor suppressor protein OPCML potentiates anti-EGFR and anti-HER2 targeted therapy in HER2-positive ovarian and breast cancer., Molecular Cancer Therapeutics, Vol: 16, Pages: 2246-2256, ISSN: 1535-7163

OPCML is a tumor suppressor gene that is frequently inactivated in ovarian cancer and many other cancers by somatic methylation. We have previously shown that OPCML exerts its suppressor function by negatively regulating a spectrum of receptor tyrosine kinases (RTKs), such as ErbB2/HER2, FGFR1 and EphA2, thus attenuating their related downstream signaling. The physical interaction of OPCML with this defined group of RTKs is a prerequisite for their downregulation. Overexpression/gene amplification of EGFR and HER2 is a frequent event in multiple cancers including ovarian and breast cancers. Molecular therapeutics against EGFR/HER2 or EGFR only, such as lapatinib and erlotinib respectively, were developed to target these receptors but resistance often occurs in relapsing cancers. Here we show that, though OPCML interacts only with HER2 and not with EGFR, the interaction of OPCML with HER2 disrupts the formation of the HER2-EGFR heterodimer and this translates into a better response to both lapatinib and erlotinib in HER2-expressing ovarian and breast cancer cell lines. Also, we show that high OPCML expression is associated with better response to lapatinib therapy in breast cancer patients and better survival in HER2-overexpressing ovarian cancer patients, suggesting that OPCML co-therapy could be a valuable sensitizing approach to RTK inhibitors.

Journal article

Antony J, Zanini E, Kelly Z, Huang R, Thiery J, Gabra H, Recchi Cet al., 2017, The phosphatase PTPRG inactivates AXL? sequestered in membrane lipid domains by the tumor suppressor OPCML., Annual Joint Meeting of the American-Society-for-Cell-Biology and the European-Molecular-Biology-Organization (ASCB/EMBO), Publisher: AMER SOC CELL BIOLOGY, ISSN: 1059-1524

Conference paper

Antony J, Tan TZ, Kelly Z, Low J, Choolani M, Recchi C, Gabra H, Thiery JP, Huang RY-Jet al., 2016, The GAS6-AXL signaling network is a mesenchymal (Mes) molecular subtype-specific therapeutic target for ovarian cancer, Science Signaling, Vol: 9, ISSN: 1945-0877

Ovarian cancer is a complex disease with heterogeneity among the gene expression molecular subtypes (GEMS) between patients. Patients with tumors of a mesenchymal (“Mes”) subtype have a poorer prognosis than patients with tumors of an epithelial (“Epi”) subtype. We evaluated GEMS of ovarian cancer patients for molecular signaling profiles and assessed how the differences in these profiles could be leveraged to improve patient clinical outcome. Kinome enrichment analysis identified AXL as a particularly abundant kinase in Mes-subtype tumor tissue and cell lines. In Mes cells, upon activation by its ligand GAS6, AXL coclustered with and transactivated the receptor tyrosine kinases (RTKs) cMET, EGFR, and HER2, producing sustained extracellular signal–regulated kinase (ERK) activation. In Epi-A cells, AXL was less abundant and induced a transient activation of ERK without evidence of RTK transactivation. AXL-RTK crosstalk also stimulated sustained activation of the transcription factor FRA1, which correlated with the induction of the epithelial-mesenchymal transition (EMT)–associated transcription factor SLUG and stimulation of motility exclusively in Mes-subtype cells. The AXL inhibitor R428 attenuated RTK and ERK activation and reduced cell motility in Mes cells in culture and reduced tumor growth in a chick chorioallantoic membrane model. A higher concentration of R428 was needed to inhibit ERK activation and cell motility in Epi-A cells. Silencing AXL in Mes-subtype cells reversed the mesenchymal phenotype in culture and abolished tumor formation in an orthotopic xenograft mouse model. Thus, AXL-targeted therapy may improve clinical outcome for patients with Mes-subtype ovarian cancer.

Journal article

Zhao W, Jamshidiha M, Lanyon-Hogg T, Recchi C, Cota E, Tate EWet al., 2016, Direct targeting of the Ras GTPase superfamily through structure-based design, Current Topics in Medicinal Chemistry, Vol: 16, Pages: 16-29, ISSN: 1873-4294

The Ras superfamily of small monomeric GTPases includes some of the most prominent cancer targets for which no selective therapeutic agent has yet been successfully developed. The turn of the millennium saw a resurgence of efforts to target these enzymes using new and improved biophysical techniques to overcome the perceived difficulties of insurmountably high affinity for guanosine nucleotides and flat, flexible topology lacking suitable pockets for small molecule inhibitors. Further, recent investigations have begun to probe the dynamic conformational status of GTP-bound Ras, opening up new mechanisms of inhibition. While much of the literature has focused on the oncogenic Ras proteins, particularly K-Ras, these represent only a small minority of therapeutically interesting targets within the superfamily; for example, the Rab GTPases are the largest subfamily of about 70 members, and present an as yet untapped class of potential targets. The present review documents the key methodologies employed to date in structure-guided attempts to drug the Ras GTPases, and forecasts their transferability to other similarly challenging proteins in the superfamily.

Journal article

Huang RY-J, Antony J, Tan TZ, Kelly Z, Gabra H, Recchi C, Thiery JPet al., 2016, Sustained Gas6/AXL signaling network in the mes subtype of ovarian cancer as a molecular subtype specific therapeutic target., Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO), Publisher: AMER SOC CLINICAL ONCOLOGY, ISSN: 0732-183X

Conference paper

Matassa DS, Amoroso MR, Lu H, Avolio R, Arzeni D, Procaccini C, Faicchia D, Maddalena F, Simeon V, Agliarulo I, Zanini E, Mazzoccoli C, Recchi C, Stronach E, Marone G, Gabra H, Matarese G, Landriscina M, Esposito Fet al., 2016, Oxidative metabolism drives inflammation-induced platinum resistance in human ovarian cancer, Cell Death and Differentiation, Vol: 23, Pages: 1542-1554, ISSN: 1476-5403

Tumour cells have long been considered defective in mitochondrial respiration and mostly dependent on glycolytic metabolism. However, this assumption is currently challenged by several lines of evidence in a growing number of tumours. Ovarian cancer (OC) is one of the most lethal cancers worldwide, but it continues to be a poorly understood disease and its metabolic features are far to be elucidated. In this context, we investigated the role of tumour necrosis factor receptor-associated protein 1 (TRAP1), which is found upregulated in several cancer types and is a key modulator of tumour cell metabolism. Surprisingly, we found that TRAP1 expression inversely correlated with grade, stage and lower survival in a large cohort of OC patients. Accordingly, TRAP1 silencing induced resistance to cisplatin, resistant cells showed increased oxidative metabolism compared with their sensitive counterpart, and the bioenergetics cellular index of higher grade tumours indicated increased mitochondrial respiration. Strikingly, cisplatin resistance was reversible upon pharmacological inhibition of mitochondrial oxidative phosphorylation by metformin/oligomycin. At molecular level, increased oxidative metabolism in low TRAP1-expressing OC cells and tissues enhanced production of inflammatory mediators such as interleukin (IL)-6 and IL-8. Mechanistically, we identified members of the multidrug resistance complex (MDR) as key mediators of such metabolism-driven, inflammation-induced process. Indeed, treatment of OC cell lines with TNFα and IL6 induced a selective increase in the expression of TAP1 and multidrug resistance protein 1, whereas TAP1 silencing sensitized cells to cisplatin-induced apoptosis. Our results unveil a novel role for TRAP1 and oxidative metabolism in cancer progression and suggest the targeting of mitochondrial bioenergetics to increase cisplatin efficacy in human OC.Cell Death and Differentiation advance online publication, 20 May 2016; doi:10.1038/cdd.201

Journal article

Booth AE, Tarafder AK, Hume AN, Recchi C, Seabra MCet al., 2016, Correction: A Role for Na+,K+-ATPase α1 in Regulating Rab27a Localisation on Melanosomes., PLOS One, Vol: 11, ISSN: 1932-6203

[This corrects the article DOI: 10.1371/journal.pone.0102851.].

Journal article

Antony J, Tan TZ, Paterson A, Recchi C, Gabra H, Thiery JP, Huang RY-Jet al., 2015, The receptor tyrosine kinase AXL modulates oncogenic signaling and epithelial mesenchymal transition in epithelial ovarian cancer, 10th Biennial Ovarian Cancer Research Symposium, Publisher: AMER ASSOC CANCER RESEARCH, ISSN: 1078-0432

Conference paper

Filipovic A, Lombardo Y, Faronato M, Abrahams J, Aboagye E, Quang-De N, d'Aqua BB, Ridley A, Green A, Rahka E, Ellis I, Recchi C, Przulj N, Sarajlic A, Alattia J-R, Fraering P, Deonarain M, Coombes RCet al., 2014, Anti-nicastrin monoclonal antibodies elicit pleiotropic anti-tumour pharmacological effects in invasive breast cancer cells (vol 148, pg 455, 2014), BREAST CANCER RESEARCH AND TREATMENT, Vol: 148, Pages: 463-463, ISSN: 0167-6806

Journal article

Filipovic A, Lombardo Y, Fronato M, Abrahams J, Aboagye E, Quang-De N, d'Aqua BB, Ridley A, Green A, Rahka E, Ellis I, Recchi C, Przulj N, Sarajlic A, Alattia J-R, Fraering P, Deonarain M, Coombes RCet al., 2014, Anti-nicastrin monoclonal antibodies elicit pleiotropic anti-tumour pharmacological effects in invasive breast cancer cells, BREAST CANCER RESEARCH AND TREATMENT, Vol: 148, Pages: 455-462, ISSN: 0167-6806

Journal article

Booth AEG, Tarafder AK, Hume AN, Recchi C, Seabra MCet al., 2014, A Role for Na+, K+-ATPase alpha 1 in Regulating Rab27a Localisation on Melanosomes, PLOS One, Vol: 9, ISSN: 1932-6203

The mechanism(s) by which Rab GTPases are specifically recruited to distinct intracellular membranes remains elusive. Herewe used Rab27a localisation onto melanosomes as a model to investigate Rab targeting. We identified the a1 subunit ofNa+,K+-ATPase (ATP1a1) as a novel Rab27a interacting protein in melanocytes and showed that this interaction is direct withthe intracellular M4M5 loop of ATP1a1 and independent of nucleotide bound status of the Rab. Knockdown studies inmelanocytes revealed that ATP1a1 plays an essential role in Rab27a-dependent melanosome transport. Specifically,expression of ATP1a1, like the Rab27a GDP/GTP exchange factor (Rab3GEP), is essential for targeting and activation ofRab27a to melanosomes. Finally, we showed that the ability of Rab27a mutants to target to melanosomes correlates withthe efficiency of their interaction with ATP1a1. Altogether these studies point to a new role for ATP1a1 as a regulator ofRab27a targeting and activation.

Journal article

Eltom S, Dale N, Raemdonck KRG, Stevenson CS, Snelgrove RJ, Sacitharan PK, Recchi C, Wavre-Shapton S, McAuley DF, O'Kane C, Belvisi MG, Birrell MAet al., 2014, Respiratory Infections Cause the Release of Extracellular Vesicles: Implications in Exacerbation of Asthma/COPD, PLOS One, Vol: 9, ISSN: 1932-6203

BackgroundInfection-related exacerbations of respiratory diseases are a major health concern; thus understanding the mechanisms driving them is of paramount importance. Despite distinct inflammatory profiles and pathological differences, asthma and COPD share a common clinical facet: raised airway ATP levels. Furthermore, evidence is growing to suggest that infective agents can cause the release of extracellular vesicle (EVs) in vitro and in bodily fluids. ATP can evoke the P2X7/caspase 1 dependent release of IL-1β/IL-18 from EVs; these cytokines are associated with neutrophilia and are increased during exacerbations. Thus we hypothesized that respiratory infections causes the release of EVs in the airway and that the raised ATP levels, present in respiratory disease, triggers the release of IL-1β/IL-18, neutrophilia and subsequent disease exacerbations.MethodsTo begin to test this hypothesis we utilised human cell-based assays, ex vivo murine BALF, in vivo pre-clinical models and human samples to test this hypothesis.ResultsData showed that in a murine model of COPD, known to have increased airway ATP levels, infective challenge causes exacerbated inflammation. Using cell-based systems, murine models and samples collected from challenged healthy subjects, we showed that infection can trigger the release of EVs. When exposed to ATP the EVs release IL-1β/IL-18 via a P2X7/caspase-dependent mechanism. Furthermore ATP challenge can cause a P2X7 dependent increase in LPS-driven neutrophilia.ConclusionsThis preliminary data suggests a possible mechanism for how infections could exacerbate respiratory diseases and may highlight a possible signalling pathway for drug discovery efforts in this area.

Journal article

Singh RK, Mizuno K, Wasmeier C, Wavre-Shapton ST, Recchi C, Catz SD, Futter C, Tolmachova T, Hume AN, Seabra MCet al., 2013, Distinct and opposing roles for Rab27a/Mlph/MyoVa and Rab27b/Munc13-4 in mast cell secretion, FEBS JOURNAL, Vol: 280, Pages: 892-903, ISSN: 1742-464X

Journal article

Eltom S, Dale N, Raemdonck K, Stevenson CS, Snelgrove R, Sacitharan PK, Recchi C, Belvisi MG, Birrell MAet al., 2013, Role Of Extracellular Vesicles In The Exacerbations Of Asthma And COPD, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 187, ISSN: 1073-449X

Journal article

Recchi C, Seabra MC, 2012, Novel functions for Rab GTPases in multiple aspects of tumour progression, Biochemical Society Transactions, Vol: 40, Pages: 1398-1403, ISSN: 1470-8752

Rab GTPases are master regulators of intracellular trafficking and, in recent years, their role in the control of different aspects of tumour progression has emerged. In the present review, we show that Rab GTPases are disregulated in many cancers and have central roles in tumour cell migration, invasion, proliferation, communication with stromal cells and the development of drug resistance. As a consequence, Rab proteins may be novel potential candidates for the development of anticancer drugs and, in this context, the preliminary results obtained with an inhibitor of Rab function are also discussed.

Journal article

Bobrie A, Krumeich S, Reyal F, Recchi C, Moita LF, Seabra MC, Ostrowski M, Thery Cet al., 2012, Rab27a Supports Exosome-Dependent and -Independent Mechanisms That Modify the Tumor Microenvironment and Can Promote Tumor Progression, CANCER RESEARCH, Vol: 72, Pages: 4920-4930, ISSN: 0008-5472

Journal article

Singh RK, Liao W, Tracey-White D, Recchi C, Tolmachova T, Rankin SM, Hume AN, Seabra MCet al., 2012, Rab27a-mediated protease release regulates neutrophil recruitment by allowing uropod detachment, JOURNAL OF CELL SCIENCE, Vol: 125, Pages: 1652-1656, ISSN: 0021-9533

Journal article

Steffen A, Le Dez G, Poincloux R, Recchi C, Nassoy P, Rottner K, Galli T, Chavrier Pet al., 2008, MT1-MMP-dependent invasion is regulated by TI-VAMP/VAMP7, CURRENT BIOLOGY, Vol: 18, Pages: 926-931, ISSN: 0960-9822

Journal article

Sakurai-Yageta M, Recchi C, Le Dez G, Sibarita J-B, Daviet L, Camonis J, D'Souza-Schorey C, Chavrier Pet al., 2008, The interaction of IQGAP1 with the exocyst complex is required for tumor cell invasion downstream of Cdc42 and RhoA, JOURNAL OF CELL BIOLOGY, Vol: 181, Pages: 985-998, ISSN: 0021-9525

Journal article

Recchi C, Chavrier P, 2006, V-ATPase: a potential pH sensor, NATURE CELL BIOLOGY, Vol: 8, Pages: 107-109, ISSN: 1465-7392

Journal article

Recchi C, Sclavi B, Rauzier J, Gicquel B, Reyrat JMet al., 2003, <i>Mycobacterium tuberculosis</i> Rv1395 is a class III transcriptional regulator of the AraC family involved in cytochrome P450 regulation, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 278, Pages: 33763-33773, ISSN: 0021-9258

Journal article

de Mendonça-Lima L, Bordat Y, Pivert E, Recchi C, Neyrolles O, Maitournam A, Gicquel B, Reyrat JMet al., 2003, The allele encoding the mycobacterial Erp protein affects lung disease in mice, CELLULAR MICROBIOLOGY, Vol: 5, Pages: 65-73, ISSN: 1462-5814

Journal article

Recchi C, Rauzier J, Gicquel B, Reyrat JMet al., 2002, Signal-sequence-independent secretion of the staphylococcal nuclease in <i>Mycobacterium smegmatis</i>, MICROBIOLOGY-SGM, Vol: 148, Pages: 529-536, ISSN: 1350-0872

Journal article

Vitale G, Pellizzari R, Recchi C, Napolitani G, Mock W, Montecucco Cet al., 1999, Anthrax lethal factor cleaves the N-terminus of MAPKKS and induces tyrosine/threonine phosphorylation of MAPKS in cultured macrophages, JOURNAL OF APPLIED MICROBIOLOGY, Vol: 87, Pages: 288-288, ISSN: 1364-5072

Journal article

Vitale G, Pellizzari R, Recchi C, Napolitani G, Mock M, Montecucco Cet al., 1998, Anthrax lethal factor cleaves the N-terminus of MAPKKs and induces tyrosine/threonine phosphorylation of MAPKs in cultured macrophages, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol: 248, Pages: 706-711, ISSN: 0006-291X

Journal article

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