ORCID Profile
0000-0002-5109-9069
Current Organisation
University of New South Wales
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In Research Link Australia (RLA), "Research Topics" refer to ANZSRC FOR and SEO codes. These topics are either sourced from ANZSRC FOR and SEO codes listed in researchers' related grants or generated by a large language model (LLM) based on their publications.
Organic Chemistry | Structural Chemistry | Biological And Medical Chemistry | Analytical Biochemistry | Organic Chemical Synthesis | Organic Chemical Synthesis | Biologically Active Molecules | Characterisation Of Macromolecules | Physical Chemistry (Incl. Structural) |
Biological sciences | Chemical sciences | Expanding Knowledge in the Chemical Sciences | Treatments (e.g. chemicals, antibiotics)
Publisher: Elsevier BV
Date: 04-2008
Publisher: Elsevier BV
Date: 04-2006
Publisher: Georg Thieme Verlag KG
Date: 23-02-2016
Publisher: Frontiers Media SA
Date: 27-06-2023
Publisher: Springer Science and Business Media LLC
Date: 16-11-2016
DOI: 10.1038/SREP37297
Abstract: Protein phosphatase 2A (PP2A) activity can be enhanced pharmacologically by PP2A-activating drugs (PADs). The sphingosine analog FTY720 is the best known PAD and we have shown that FTY720 represses production of pro-inflammatory cytokines responsible for respiratory disease pathogenesis. Whether its phosphorylated form, FTY720-P, also enhances PP2A activity independently of the sphingosine 1-phosphate (S1P) pathway was unknown. Herein, we show that FTY720-P enhances TNF-induced PP2A phosphatase activity and significantly represses TNF-induced interleukin 6 (IL-6) and IL-8 mRNA expression and protein secretion from A549 lung epithelial cells. Comparing FTY720 and FTY720-P with S1P, we show that unlike S1P, the sphingosine analogs do not induce cytokine production on their own. In fact, FTY720 and FTY720-P significantly repress S1P-induced IL-6 and IL-8 production. We then examined their impact on expression of cyclooxygenase 2 (COX-2) and resultant prostaglandin E 2 (PGE 2) production. S1P did not increase production of this pro-inflammatory enzyme because COX-2 mRNA gene expression is NF-κB-dependent, and unlike TNF, S1P did not activate NF-κB. However, TNF-induced COX-2 mRNA expression and PGE 2 secretion is repressed by FTY720 and FTY720-P. Hence, FTY720-P enhances PP2A activity and that PADs can repress production of pro-inflammatory cytokines and enzymes in A549 lung epithelial cells in a manner devoid of S1P agonism.
Publisher: Royal Society of Chemistry (RSC)
Date: 2013
DOI: 10.1039/C3RP00011G
Publisher: American Chemical Society (ACS)
Date: 19-01-2011
DOI: 10.1021/OM1010885
Publisher: Springer Science and Business Media LLC
Date: 20-01-2013
DOI: 10.1038/NM.3049
Abstract: Allergic airway inflammation is associated with activation of innate immune pathways by allergens. Acute exacerbations of asthma are commonly associated with rhinovirus infection. Here we show that, after exposure to house dust mite (HDM) or rhinovirus infection, the E3 ubiquitin ligase midline 1 (MID1) is upregulated in mouse bronchial epithelium. HDM regulates MID1 expression in a Toll-like receptor 4 (TLR4)- and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-dependent manner. MID1 decreases protein phosphatase 2A (PP2A) activity through association with its catalytic subunit PP2Ac. siRNA-mediated knockdown of MID1 or pharmacological activation of PP2A using a nonphosphorylatable FTY720 analog in mice exposed to HDM reduces airway hyperreactivity and inflammation, including the expression of interleukin-25 (IL-25), IL-33 and CCL20, IL-5 and IL-13 release, nuclear factor (NF)κB activity, p38 mitogen-activated protein kinase (MAPK) phosphorylation, accumulation of eosinophils, T lymphocytes and myeloid dendritic cells, and the number of mucus-producing cells. MID1 inhibition also limited rhinovirus-induced exacerbation of allergic airway disease. We found that MID1 was upregulated in primary human bronchial epithelial cells upon HDM or rhinovirus exposure, and this correlated with TRAIL and CCL20 expression. Together, these findings identify a key role of MID1 in allergic airway inflammation and links innate immune pathway activation to the development and exacerbation of asthma.
Publisher: Springer Science and Business Media LLC
Date: 08-04-2202
Publisher: Wiley
Date: 04-05-2017
Publisher: Springer Science and Business Media LLC
Date: 20-02-2017
DOI: 10.1038/ONC.2017.2
Publisher: American Chemical Society (ACS)
Date: 08-03-2002
DOI: 10.1021/JO015887B
Publisher: American Chemical Society (ACS)
Date: 23-04-2009
DOI: 10.1021/CG9002302
Publisher: Wiley
Date: 21-06-2017
DOI: 10.1111/ALL.13212
Abstract: Asthma is an allergic airway disease (AAD) caused by aberrant immune responses to allergens. Protein phosphatase-2A (PP2A) is an abundant serine/threonine phosphatase with anti-inflammatory activity. The ubiquitin proteasome system (UPS) controls many cellular processes, including the initiation of inflammatory responses by protein degradation. We assessed whether enhancing PP2A activity with fingolimod (FTY720) or 2-amino-4-(4-(heptyloxy) phenyl)-2-methylbutan-1-ol (AAL Acute AAD was induced in C57BL/6 mice by intraperitoneal sensitization with ovalbumin (OVA) in combination with intranasal (i.n) exposure to OVA. Chronic AAD was induced in mice with prolonged i.n exposure to crude house dust mite (HDM) extract. Mice were treated with vehicle, FTY720, AAL AAL These findings highlight the potential of combination therapies that enhance PP2A and inhibit proteasome activity as novel therapeutic strategies for asthma.
Publisher: Royal Society of Chemistry (RSC)
Date: 2009
DOI: 10.1039/B805111A
Publisher: Elsevier BV
Date: 08-2015
DOI: 10.1016/J.JACI.2014.11.044
Abstract: Steroid-resistant asthma is a major clinical problem that is linked to activation of innate immune cells. Levels of IFN-γ and LPS are often increased in these patients. Cooperative signaling between IFN-γ/LPS induces macrophage-dependent steroid-resistant airway hyperresponsiveness (AHR) in mouse models. MicroRNAs (miRs) are small noncoding RNAs that regulate the function of innate immune cells by controlling mRNA stability and translation. Their role in regulating glucocorticoid responsiveness and AHR remains unexplored. IFN-γ and LPS synergistically increase the expression of miR-9 in macrophages and lung tissue, suggesting a role in the mechanisms of steroid resistance. Here we demonstrate the role of miR-9 in IFN-γ/LPS-induced inhibition of dexamethasone (DEX) signaling in macrophages and in induction of steroid-resistant AHR. MiRNA-9 expression was assessed by means of quantitative RT-PCR. Putative miR-9 targets were determined in silico and confirmed in luciferase reporter assays. miR-9 function was inhibited with sequence-specific antagomirs. The efficacy of DEX was assessed by quantifying glucocorticoid receptor (GR) cellular localization, protein phosphatase 2A (PP2A) activity, and AHR. Exposure of pulmonary macrophages to IFN-γ/LPS synergistically induced miR-9 expression reduced levels of its target transcript, protein phosphatase 2 regulatory subunit B (B56) δ isoform attenuated PP2A activity and inhibited DEX-induced GR nuclear translocation. Inhibition of miR-9 increased both PP2A activity and GR nuclear translocation in macrophages and restored steroid sensitivity in multiple models of steroid-resistant AHR. Pharmacologic activation of PP2A restored DEX efficacy and inhibited AHR. MiR-9 expression was increased in sputum of patients with neutrophilic but not those with eosinophilic asthma. MiR-9 regulates GR signaling and steroid-resistant AHR. Targeting miR-9 function might be a novel approach for the treatment of steroid-resistant asthma.
Publisher: Elsevier BV
Date: 04-2016
DOI: 10.1016/J.BMC.2016.02.016
Abstract: A flexible and efficient synthesis of the neuroprotective alkaloid, dictyoquinazol A, is reported. Several structural analogues of the target molecule were produced, and the neuroprotective activity of this series of compounds was investigated using three different cell-based models of stroke. Several of the new compounds were found to have superior activity compared to the natural product. This work has established a new molecular scaffold that holds promise for a novel pharmaceutical treatment for stroke.
Publisher: American Chemical Society (ACS)
Date: 31-01-2008
DOI: 10.1021/JM700940H
Publisher: Wiley
Date: 04-05-2017
Abstract: The first total synthesis of the potent antimalarial 7,3'-linked naphthylisoquinoline alkaloid dioncophylline E (1) has been completed. The synthesis proceeds in 12 steps (longest linear sequence) and in 15 % overall yield. Key transformations include an ortho-arylation of a naphthol with an aryllead triacetate to construct the sterically hindered biaryl bond, and a three-step sequence to stereoselectively generate the trans-1,3-dimethyl-1,2,3,4-tetrahydroisoquinoline moiety.
Publisher: American Chemical Society (ACS)
Date: 15-07-2005
DOI: 10.1021/JO050523V
Publisher: American Society for Pharmacology & Experimental Therapeutics (ASPET)
Date: 07-07-2010
Publisher: Elsevier BV
Date: 04-2016
DOI: 10.1016/J.CELLSIG.2016.01.009
Abstract: Chronic respiratory diseases are driven by inflammation, but some clinical conditions (severe asthma, COPD) are refractory to conventional anti-inflammatory therapies. Thus, novel anti-inflammatory strategies are necessary. The mRNA destabilizing protein, tristetraprolin (TTP), is an anti-inflammatory molecule that functions to induce mRNA decay of cytokines that drive pathogenesis of respiratory disorders. TTP is regulated by phosphorylation and protein phosphatase 2A (PP2A) is responsible for dephosphorylating (and hence activating) TTP, amongst other targets. PP2A is activated by small molecules, FTY720 and AAL(S), and in this study we examine whether these compounds repress cytokine production in a cellular model of airway inflammation using A549 lung epithelial cells stimulated with tumor necrosis factor α (TNFα) in vitro. PP2A activators significantly increase TNFα-induced PP2A activity and inhibit mRNA expression and protein secretion of interleukin 8 (IL-8) and IL-6 two key pro-inflammatory cytokines implicated in respiratory disease and TTP targets. The effect of PP2A activators is not via an increase in TNFα-induced TTP mRNA expression instead we demonstrate a link between PP2A activation and TTP anti-inflammatory function by showing that specific knockdown of TTP with siRNA reversed the repression of TNFα-induced IL-8 and IL-6 mRNA expression and protein secretion by FTY720. Therefore we propose that PP2A activators affect the dynamic equilibrium regulating TTP shifting the equilibrium from phosphorylated (inactive) towards unphosphorylated (active) but unstable TTP. PP2A activators boost the anti-inflammatory function of TTP and have implications for future pharmacotherapeutic strategies to combat inflammation in respiratory disease.
Publisher: Cold Spring Harbor Laboratory
Date: 12-03-2023
DOI: 10.1101/2023.03.10.532020
Abstract: Insulin resistance (IR) is a complex metabolic disorder that underlies several human diseases, including type 2 diabetes and cardiovascular disease. Despite extensive research, the precise mechanisms underlying IR development remain poorly understood. Here, we provide new insights into the mechanistic connections between cellular alterations associated with IR, including increased ceramides, deficiency of coenzyme Q (CoQ), mitochondrial dysfunction, and oxidative stress. We demonstrate that elevated levels of ceramide in the mitochondria of skeletal muscle cells results in CoQ depletion and loss of mitochondrial respiratory chain components, leading to mitochondrial dysfunction and IR. Further, decreasing mitochondrial ceramide levels in vitro and in animal models increased CoQ levels and was protective against IR. CoQ supplementation also rescued ceramide-associated IR. Examination of the mitochondrial proteome from human muscle biopsies revealed a strong correlation between the respirasome system and mitochondrial ceramide as key determinants of insulin sensitivity. Our findings highlight the mitochondrial Ceramide-CoQ-respiratory chain nexus as a potential foundation of an IR pathway that may also play a critical role in other conditions associated with ceramide accumulation and mitochondrial dysfunction, such as heart failure, cancer, and aging. These insights may have important clinical implications for the development of novel therapeutic strategies for the treatment of IR and related metabolic disorders.
Publisher: CSIRO Publishing
Date: 2014
DOI: 10.1071/CH14205
Abstract: Two new fluorescent ruthenium(iii) complexes, namely 7-azaindolium trans-tetrachlorido(7-azaindole)(dimethylsulfoxide)ruthen(iii)ate (F1) and N-[histaminedihydrolium]-1,8-naphthalenecarboximidic trans-tetracholoro(dimethylsulfoxide)(N-[histaminedihydro]-1,8-naphthalenecarboximide)ruthen(iii)ate (F2) and their respective tetramethylammonium analogues (F3 and F4) are reported herein. The compounds were characterised by elemental analysis, mass spectrometry, UV-vis spectrophotometry, and fluorescence spectroscopy. Molar extinction coefficients (ϵmax) and fluorescence emission spectra were compared to evaluate the electronic properties of the synthesised fluorescent analogues, and hence their value as intracellular fluorescence probes. F3 and F4 were synthesised and characterised in order to eliminate fluorescence arising from the counter-cations in F1 and F2 and thus to obtain a fluorescence quantum yield that reflects only a contribution from the metal complex anion. Half-inhibitory concentrations (IC50) were determined for A549 cells exposed to the Ru complexes for 24 h: F3 (203 ± 26 μM) and F4 (185 ± 20 μM).
Publisher: Elsevier BV
Date: 12-2001
Publisher: Wiley
Date: 2019
DOI: 10.1002/CTI2.1084
Abstract: Chronic obstructive pulmonary disease (COPD) is a progressive disease that causes significant mortality and morbidity worldwide and is primarily caused by the inhalation of cigarette smoke (CS). Lack of effective treatments for COPD means there is an urgent need to identify new therapeutic strategies for the underlying mechanisms of pathogenesis. Tristetraprolin (TTP) encoded by the Zfp36 gene is an anti‐inflammatory protein that induces mRNA decay, especially of transcripts encoding inflammatory cytokines, including those implicated in COPD. Here, we identify a novel protective role for TTP in CS‐induced experimental COPD using Zfp36 aa/aa mice, a genetically modified mouse strain in which endogenous TTP cannot be phosphorylated, rendering it constitutively active as an mRNA‐destabilising factor. TTP wild‐type ( Zfp36 +/+ ) and Zfp36 aa/aa active C57BL/6J mice were exposed to CS for four days or eight weeks, and the impact on acute inflammatory responses or chronic features of COPD, respectively, was assessed. After four days of CS exposure, Zfp36 aa/aa mice had reduced numbers of airway neutrophils and lymphocytes and mRNA expression levels of cytokines compared to wild‐type controls. After eight weeks, Zfp36 aa/aa mice had reduced pulmonary inflammation, airway remodelling and emphysema‐like alveolar enlargement, and lung function was improved. We then used pharmacological treatments in vivo (protein phosphatase 2A activator, AAL (S) , and the proteasome inhibitor, bortezomib) to promote the activation and stabilisation of TTP and show that hallmark features of CS‐induced experimental COPD were ameliorated. Collectively, our study provides the first evidence for the therapeutic potential of inducing TTP as a treatment for COPD.
Publisher: American Association for Cancer Research (AACR)
Date: 09-2007
Publisher: Elsevier BV
Date: 2003
Publisher: Springer Science and Business Media LLC
Date: 19-12-2018
DOI: 10.1038/S41467-018-07620-0
Abstract: We recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of acute myeloid leukemia (AML). Here, we show that genetic or pharmacological inhibition of SRPK1 leads to cell cycle arrest, leukemic cell differentiation and prolonged survival of mice transplanted with MLL -rearranged AML. RNA-seq analysis demonstrates that SRPK1 inhibition leads to altered isoform levels of many genes including several with established roles in leukemogenesis such as MYB , BRD4 and MED24 . We focus on BRD4 as its main isoforms have distinct molecular properties and find that SRPK1 inhibition produces a significant switch from the short to the long isoform at the mRNA and protein levels. This was associated with BRD4 eviction from genomic loci involved in leukemogenesis including BCL2 and MYC . We go on to show that this switch mediates at least part of the anti-leukemic effects of SRPK1 inhibition. Our findings reveal that SRPK1 represents a plausible new therapeutic target against AML.
Publisher: Elsevier BV
Date: 12-2011
Publisher: Elsevier BV
Date: 06-2014
DOI: 10.1016/J.JACI.2013.11.014
Abstract: β-Agonists are used for relief and control of asthma symptoms by reversing bronchoconstriction. They might also have anti-inflammatory properties, but the underpinning mechanisms remain poorly understood. Recently, a direct interaction between formoterol and protein phosphatase 2A (PP2A) has been described in vitro. We sought to elucidate the molecular mechanisms by which β-agonists exert anti-inflammatory effects in allergen-driven and rhinovirus 1B-exacerbated allergic airways disease (AAD). Mice were sensitized and then challenged with house dust mite to induce AAD while receiving treatment with salmeterol, formoterol, or salbutamol. Mice were also infected with rhinovirus 1B to exacerbate lung inflammation and therapeutically administered salmeterol, dexamethasone, or the PP2A-activating drug (S)-2-amino-4-(4-[heptyloxy]phenyl)-2-methylbutan-1-ol (AAL[S]). Systemic or intranasal administration of salmeterol protected against the development of allergen- and rhinovirus-induced airway hyperreactivity and decreased eosinophil recruitment to the lungs as effectively as dexamethasone. Formoterol and salbutamol also showed anti-inflammatory properties. Salmeterol, but not dexamethasone, increased PP2A activity, which reduced CCL11, CCL20, and CXCL2 expression and reduced levels of phosphorylated extracellular signal-regulated kinase 1 and active nuclear factor κB subunits in the lungs. The anti-inflammatory effect of salmeterol was blocked by targeting the catalytic subunit of PP2A with small RNA interference. Conversely, increasing PP2A activity with AAL(S) abolished rhinovirus-induced airway hyperreactivity, eosinophil influx, and CCL11, CCL20, and CXCL2 expression. Salmeterol also directly activated immunoprecipitated PP2A in vitro isolated from human airway epithelial cells. Salmeterol exerts anti-inflammatory effects by increasing PP2A activity in AAD and rhinovirus-induced lung inflammation, which might potentially account for some of its clinical benefits.
Publisher: American Chemical Society (ACS)
Date: 19-08-2006
DOI: 10.1021/JO0611364
Publisher: American Chemical Society (ACS)
Date: 10-1997
DOI: 10.1021/JO970873K
Publisher: Springer Science and Business Media LLC
Date: 03-2006
Publisher: American Chemical Society (ACS)
Date: 1996
DOI: 10.1021/JA9537888
Publisher: Impact Journals, LLC
Date: 18-06-2016
Publisher: Royal Society of Chemistry (RSC)
Date: 2015
DOI: 10.1039/C5OB01931A
Abstract: This work has led to the identification of a selective CerS1 inhibitor that is non-cytotoxic.
Publisher: Cold Spring Harbor Laboratory
Date: 06-08-2023
Publisher: Royal Society of Chemistry (RSC)
Date: 2016
DOI: 10.1039/C6OB00556J
Abstract: The synthesis and biological evaluation of new cytotoxic analogs of AAL(S) are reported. Our findings identify key structural motifs required for anti-cancer effects.
Publisher: Elsevier BV
Date: 08-2012
DOI: 10.1194/JLR.D025627
Publisher: American Physiological Society
Date: 06-2022
Publisher: Royal Society of Chemistry (RSC)
Date: 2009
DOI: 10.1039/B821368B
Publisher: American Society for Pharmacology & Experimental Therapeutics (ASPET)
Date: 29-12-2016
Publisher: Royal Society of Chemistry (RSC)
Date: 2013
DOI: 10.1039/C3NP20116C
Publisher: American Chemical Society (ACS)
Date: 16-01-2002
DOI: 10.1021/OL017258U
Publisher: Springer Science and Business Media LLC
Date: 07-02-2019
Publisher: Elsevier BV
Date: 04-2000
Publisher: International Union of Crystallography (IUCr)
Date: 15-10-2000
Publisher: American Chemical Society (ACS)
Date: 04-06-2021
Publisher: Elsevier BV
Date: 10-2011
Publisher: Springer Science and Business Media LLC
Date: 21-08-2018
DOI: 10.1038/S41467-018-05613-7
Abstract: Specific forms of the lipid ceramide, synthesized by the ceramide synthase enzyme family, are believed to regulate metabolic physiology. Genetic mouse models have established C16 ceramide as a driver of insulin resistance in liver and adipose tissue. C18 ceramide, synthesized by ceramide synthase 1 (CerS1), is abundant in skeletal muscle and suggested to promote insulin resistance in humans. We herein describe the first isoform-specific ceramide synthase inhibitor, P053, which inhibits CerS1 with nanomolar potency. Lipidomic profiling shows that P053 is highly selective for CerS1. Daily P053 administration to mice fed a high-fat diet (HFD) increases fatty acid oxidation in skeletal muscle and impedes increases in muscle triglycerides and adiposity, but does not protect against HFD-induced insulin resistance. Our inhibitor therefore allowed us to define a role for CerS1 as an endogenous inhibitor of mitochondrial fatty acid oxidation in muscle and regulator of whole-body adiposity.
Publisher: American Chemical Society (ACS)
Date: 04-1997
DOI: 10.1021/JA963935H
Publisher: American Chemical Society (ACS)
Date: 06-02-2017
DOI: 10.1021/ACSCHEMBIO.6B01048
Abstract: Serine/arginine-protein kinase 1 (SRPK1) regulates alternative splicing of VEGF-A to pro-angiogenic isoforms and SRPK1 inhibition can restore the balance of pro/antiangiogenic isoforms to normal physiological levels. The lack of potency and selectivity of available compounds has limited development of SRPK1 inhibitors, with the control of alternative splicing by splicing factor-specific kinases yet to be translated. We present here compounds that occupy a binding pocket created by the unique helical insert of SRPK1, and trigger a backbone flip in the hinge region, that results in potent (<10 nM) and selective inhibition of SRPK1 kinase activity. Treatment with these inhibitors inhibited SRPK1 activity and phosphorylation of serine/arginine splicing factor 1 (SRSF1), resulting in alternative splicing of VEGF-A from pro-angiogenic to antiangiogenic isoforms. This property resulted in potent inhibition of blood vessel growth in models of choroidal angiogenesis in vivo. This work identifies tool compounds for splice isoform selective targeting of pro-angiogenic VEGF, which may lead to new therapeutic strategies for a ersity of diseases where dysfunctional splicing drives disease development.
Publisher: Springer Science and Business Media LLC
Date: 18-05-2015
DOI: 10.1038/SREP10063
Publisher: Royal Society of Chemistry (RSC)
Date: 2011
DOI: 10.1039/C0NP00066C
Publisher: Elsevier BV
Date: 04-2014
Publisher: Royal Society of Chemistry (RSC)
Date: 2007
DOI: 10.1039/B602832M
Publisher: Elsevier BV
Date: 2002
Publisher: Elsevier BV
Date: 2009
Publisher: American Chemical Society (ACS)
Date: 17-01-2014
DOI: 10.1021/OL403390M
Publisher: American Chemical Society (ACS)
Date: 29-09-2011
DOI: 10.1021/OM200659T
Publisher: American Thoracic Society
Date: 07-2014
Publisher: Elsevier BV
Date: 07-2017
DOI: 10.1016/J.BCP.2017.03.016
Abstract: The leukocyte-derived heme enzyme myeloperoxidase (MPO) is released extracellularly during inflammation and impairs nitric oxide (NO) bioavailability by directly oxidizing NO or producing NO-consuming substrate radicals. Here, structurally erse pharmacological agents with activities as MPO substrates/inhibitors or antioxidants were screened for their effects on MPO NO oxidase activity in human plasma and physiological model systems containing endogenous MPO substrates/antioxidants (tyrosine, urate, ascorbate). Hydrazide-based irreversible/reversible MPO inhibitors (4-ABAH, isoniazid) or the sickle cell anaemia drug, hydroxyurea, all promoted MPO NO oxidase activity. This involved the capacity of NO to antagonize MPO inhibition by hydrazide-derived radicals and/or the ability of drug-derived radicals to stimulate MPO turnover thereby increasing NO consumption by MPO redox intermediates or NO-consuming radicals. In contrast, the mechanism-based irreversible MPO inhibitor 2-thioxanthine, potently inhibited MPO turnover and NO consumption. Although the phenolics acetaminophen and resveratrol initially increased MPO turnover and NO consumption, they limited the overall extent of NO loss by rapidly depleting H
Publisher: Royal Society of Chemistry (RSC)
Date: 2010
DOI: 10.1039/B919366A
Publisher: Royal Society of Chemistry (RSC)
Date: 2008
DOI: 10.1039/B701533J
Publisher: Elsevier BV
Date: 2001
Publisher: Elsevier BV
Date: 04-2008
Publisher: Royal Society of Chemistry (RSC)
Date: 2008
DOI: 10.1039/B814839B
Publisher: American Chemical Society (ACS)
Date: 02-06-2009
DOI: 10.1021/CR900032S
Start Date: 2007
End Date: 12-2009
Amount: $230,000.00
Funder: Australian Research Council
View Funded ActivityStart Date: 2017
End Date: 09-2020
Amount: $305,000.00
Funder: Australian Research Council
View Funded ActivityStart Date: 08-2009
End Date: 12-2010
Amount: $560,000.00
Funder: Australian Research Council
View Funded Activity