Dr. Talat Nasim,Associate Professor
Information about Dr. Talat Nasim at the University of Bradford.
- School of Pharmacy & Medical Sciences
(Faculty of Life Sciences) - Email:
- t.nasim@bradford.ac.uk
- Telephone:
- +44 1274 236076
Biography
CurrentlyDr. Nasim is an Associate Professor in Therapeutics at the School of Pharmacy andMedical Sciences, the University of Bradford, UK. He is an Executive Member,Research and Knowledge Transfer Committee, Faculty of Life Sciences, Universityof Bradford, Local Ambassador, the Biochemical Society, United Kingdom,Adviser, the Commonwealth Scholarship Commission, United Kingdom, ExecutiveMember, Global Network of Bangladeshi Biotechnologists (GNOBB). He has been themember of Editorial Boards of a number of international journals includingJournal of Bioscience, International Journal of Perception in Public Health andacted as a Guest Editor for the journal Pain Research and Management. His research interests focus in the broader areas ofTranslational Medicine (gene identification to drug discovery). He has identified a few key genes that causedisorders such as Pulmonary Hypertension and blood cancer and identified noveldiagnostics and therapeutics. Importantly, his discoveries are being taught atthe university level and he is the inventor of a number of diagnostic andtherapeutic patents.His contributions to science include publications inscientific journals, articles to local and national Bangladeshi dailynewspapers and intellectual supports to scientific community around the world.He has published 70 articles including research papers in journals like NatureGenetics, Nature Protocols, Nature Communications, Nucleic Acids Research,Human Molecular Genetics. His research has been extensively highlighted in newsmedia across the globe as evidenced in his interviews with CBA News (USA), Labmate https://www.labmate-online.com/news/news-and-views/5/university-of-bradford/diagnostic-clues-found-for-pah/48687 (UK) and Daily Prothom-alo(Bangladesh). He writes regularly in newspapers including the Daily New Nation (http://thedailynewnation.com/news/250850/coronavirus--our-duties-to-prevent-and-halt-the-outbreak.html), the Daily New Age (https://www.newagebd.net/article/103938/are-face-masks-effective-against-coronavirus-disease), daily Jugantor,Daily Prothom-alo, RatdinNews (à¦à¦°à§à¦¨à¦¾: লালমনিরহাà¦à§à¦° বিà¦à§à¦à¦¾à¦¨à§ নাসিমà§à¦° নিবনà§à¦§)and Lalmonirhat Barta (http://lalmonibarta.com/details.php?mblogs=ODczNQ==) and edited books inaugurated by thePrime Minister of the Peoples Republic of Bangladesh. Hehas been promoting science in Bangladesh. He is the founder and Chief Adviserof the organization called Centre for Health Agriculture and Socio-economicAdvancements (CHASA), which was incepted in 2008 at Lalmonirhat, Bangladesh.Since its inception, CHASA has provided more than 150 scholarships to localstudents at various levels from primary to college and supported researchprojects at universities which resulted in a few scientific publications. Dr.Nasim received his Ph.D degree from the University of Manchester Institute ofScience and Technology (UMIST), UK. In his student life, he received 18scholarships from various countries including Bangladesh, Switzerland, USA andUK. In fact, he is the first ever Bangladeshi student who received the SwissGovt. Scholarship. Dr.Nasim was a co-recipient of the Best Scientist Award 2008 of LalmonirhatMunicipality (Bangladesh) and received nomination for the âBest Non-residentBangladeshi Scientist-2019â of Global Network of Bangladeshi Biotechnologists(GNOBB).
Research
Prospective self-funded Ph.Dstudents interested in pursuing their research in the broader areas of Biochemistry,Molecular Genetics, Pharmacology, Drug Discovery and Translational Medicine arestrongly encouraged to contact me (t.nasim@bradford.ac.uk)with a CV. Additionally, we are supporting talented post-doctoral scientists interested in our research who want to apply for their own funding.Current PhD projects:1. Therapeutic resolution of BMPR2-mediated signalling defects in pulmonary arterial hypertension (PAH)2. Therapeutic resolution of pulmonary arterial hypertension (PAH) by natural products3. Re-purposing established drugs for the resolution of pulmonary arterial hypertension (PAH)4. Development of a personalized therapy for pulmonary arterial hypertension (PAH)5. Therapeutic resolution of coronavirus (COVID-19) diseases by natural products6. Therapeutic resolution of Myelodysplastic Syndrome (MDS) by natural productsApply for one of our PhD projects - Postgraduate - University of BradfordPotential funding sources are:Faculty for the Future FellowshipEMBO FellowshipsRoyal Society Newton International FellowshipHuman Science Frontier ProgrammeMarie Curie Individual FellowshipsCommonwealth Scholarship Commission (https://cscuk.fcdo.gov.uk/about-us/scholarships/)My key research interests are as follows:1. Investigation of BMP and TGFb signalling events to resolve pulmonary arterial hypertension (PAH)PAH is a devastating cardiovascular disorder caused by narrowing of blood vessels in the lungs and in the absence of therapy leads to right heart failure and death. We have established that nonsense mutations in the BMPR2 gene underlie the majority of the inherited forms of the disease. BMPR2 mutations contribute to stoichiometric imbalance in the receptor complex leading to dysfunctional signalling (Nasim et al., 2008, 2012). Mutations are also found in the SMAD family genes but they represent an infrequent cause of the disease (Nasim et al., 2011). Mutations in the BMPR2 gene potentiate TGFb signalling (Nasim et al., 2012) and prostacyclins, the commonly used therapy for severe PAH inhibit this pathway (Ogo et al., 2013). Taken together these observations suggest that agents that inhibit the overactive TGFb signalling and/or promote the BMP signalling may provide protection in PAH. We identified some small molecule agents that restore the balance between the TGFb and BMP pathways and rescued abnormal proliferation and apoptosis in cell-based models of PAH (Siddiqui et al., 2013). Structure guided virtual screening identified additional compounds which elicited anti-TGFb activity in cell-based assays. A number of âleadsâ have been identified through a medicinal chemistry programme (unpublished data).The major objectives of this part of research are to investigate (a) the molecular mechanisms by which the TGFb signalling is activated in PAH, and (b) therapeutic resolution of PAH by chemical agents including natural products and established drugs that restore the balance between BMP and TGFb signalling pathways.ReferencesM.T. Nasim, T. Ogo, H.M. Chowdhury and R.C. Trembath. Human Mol Genetics (doi 10.1093/hmg/DDS073), 2012M T. Nasim, T. Ogo, M. Ahmed, R. Randall, et al. Human Mutation 12:1385-89, 2011M.T. Nasim, A.G. Ghouri, B.P. Patel, et al., Hum Mol Genet (11):1683-94, 2008M. T. Nasim, S. Jaenecke, A. Belduz, et al., J. Biol. Chem. 275: 14646-14852, 2000T. Ogo, H.M. Chowdhury, N.W. Morrell, R.C. Trembath and M.T. Nasim. (American Journal of Respiratory Cell and Molecular Biology), 2013.H.M. Chowdhury, M. A. Sidiqui, S. Kanneganti, N. Sharmin and M. T. Nasim*. Hum Mol Genet.27: 373-384, 2018H.M. Chowdhury, N. Sharmin, M. Baran, L. Long, N.W. Morrell, R. C. Trembath andM. T. Nasim*.Hum Mol Genet Feb 2019M.A Siddiqui, M. Ahmed, T. Ogo, M. Hossain, H.M. Chowdhury, L.Long, F. Khan, N. W. Morrell, R.C. Trembath and M.T. Nasim (unpublished).2. Therapeutic resolution of nonsense-associated genetic disorders by promotion of translation readthroughThere are more than 3000 genetic disorders including cystic fibrosis, muscular dystrophy and PAH caused by nonsense mutations. Agents that promote translation readthorugh may provide therapeutic intervention. We have established cell based assay system which is capable of screening drugs that promote translational readthorugh (Nasim et al., 2000, 2005, 2008 and patent applications). Using these techniques, hits have been identified through screening of a small molecule library, which are now being tested whether they rescue BMPR2-mediated cellular defects in PAH.The major objectives of this part of research are to (a) identify agents that promote readthrough and (b) test whether promotion of readthrough by small molecule agents can provide protection in PAH and in other nonsense associated genetic disorders.ReferencesM.T. Nasim, A.G. Ghouri, B.P. Hum Mol Genet (11):1683-94, 2008.2. M.T. Nasim* and R.C. Trembath. Nucleic Acids Res. 33(7): e66 (8 pages), 2005. M. T. Nasim, S. Jaenecke, A. Belduz, H. Kollmus, L. Flohe and J.E.G. McCarthy; J. Biol. Chem. 275: 14646-14852, 2000.3. Modulation ofSplicing in human diseasesIdentification ofnon-canonical factors regulating tissue-specific alternative splicingMutations in pre-mRNA splicing signalsaccount for both inherited and acquired defects, are now increasinglyrecognized as causes of human diseases. Improvements of our currentunderstanding of alternative splicing regulation may therefore provideopportunities to counter the consequences of mutation. Although many componentsof the spliceosomal complex have been identified, their roles in splicingregulation (e.g. activator or inhibitor) are not fully understood. We andothers have reported the involvement of non-canonical proteins and micro-RNAs(miRNAs) in regulating splicing events, which suggest that this process iscontrolled by many more factors than previously thought. Hence, constructing agenome-wide map is essential in revealing the mechanisms involved. Identificationof such factors and the characterization of âex-vivoâ networks require a systemcapable of screening a large number of samples. The absence of a genericapproach prompted me to develop rapid assay systems based on enzymatic andfluorescence activities (Nasim et al., 2002, 2006, 2008, 2011). Each methodcomprises two distinct signals either fluorescence or luminescence which can bemonitored in mammalian cells, providing a basis for high throughput format. In this project, we seek to constructa genome-wide map for splicing regulation employing these established approachesand identify novel non-canonical factors including proteins, chemicals andmiRNAs that modulate tissue-specific alternative splicing of the human tropomyosin3 (TPM3) gene. This study will be of substantial use to the study ofalternative and aberrant splicing of a wide range of disorders, will greatlyenhance the identification of novel drug targets and therapies as well as thedevelopment of novel diagnostic tests.4. Therapeuticresolution of myelodysplastic syndrome (MDS) by modulation of aberrant splicingMyelodysplasticsyndromes (MDS) are the most common adult myeloloid malignancy in the UK and approximately 30% of patients willtransform to secondary acute myeloid leukaemia (AML), which has a poorprognosis. There is no cure for MDS and current maintenance therapies were allestablished prior to the realisation that MDS have substantial geneticcomponents. Hence, there is a need to develop a novel therapy which accountsfor the biochemical consequences of such gene defects. We have previouslydemonstrated that heterozygous missense mutations in U2AF1 (encoding U2AF35, the 35 kDacomponent of the heterodimeric U2 auxiliary factor), underlie the majority of MDS. We have demonstrated that thesemutations potentiate overactive splicing and alter downstream gene isoformexpression and therefore contribute to abnormal haematopoiesis. Our preliminarydata indicate that agents that inhibit this overactive splicing may providebeneficial effects in vitro and in vivo mouse models. The major aim of thisproject is to develop a targeted chemotherapy for MDS by inhibition ofoveractive splicing activity of pathogenic nonsense alleles using smallmolecule agents. In this project we seek to utilise and expand on ourpreliminary observations to identify small molecule agents capable of targetingU2AF1-mediated splicing defects for selective therapy. Compounds will beidentified by means of cell-based and insilico screening and validation will be performed in K562 myeloid cell linemodels and bone marrow cells derived from MDS patients.ReferencesM. T. Nasim, H. M. Chowdhury and I. C. Eperon.Nucleic Acids Res. 30: e109, 2002.M.T. Nasim and R.C. Trembath. NucleicAcids Res. 33(7): e66 (8 pages), 2005.M.T. Nasim and I. C. Eperon. NatureProtocols 1(2):1022-1028, 2006.M. T. Nasim, T. K. Chernova, H.M. Chowdhury, B.Yue and I. C. Eperon. Hum Mol Genet. 12:1337-1348, 2003.Suraweera A, Lim Y, Woods R, BirrellGW, Nasim T, Becherel OJ, Lavin MF. Hum MolGenet.(18):3384-96, 2009.Katiyar S, Maria A, Covarrubias Y,Casimiro M.C, Zhou J, Jaio X, Hyslop T, Nasim T, Fortina P,Pestell R. Cancer Research; 72(4):1023-34), 2012.T. Graubert, D Shen, T. Nasim, D. Link, M. Tomasson, P. Westervelt, J.DiPersio, E. Mardis, T. Ley, R. Wilson, and M. Walter. Nature Genetics 44(1):53-7, 2012.M. Brioschi, S. Lento, S.Barcella, M.T. Nasim, S. Ghilardi, S.Barbieri, E. Tremoli and C. Banfi. Data Brief. ;25;3:117-9, 2015§ S. Lento, M. Brioschi, S. Barcella, M.T. Nasim, S. Ghilardi, S. Barbieri, E.Tremoli and C. Banfi. J Proteomics.;119:75-89, 20155. Breast cancer gene function study of Bangladeshi populationBreast cancer (BC) is the leading cause of cancer deaths among women worldwide, with an estimated 1.7 million cases and > 0.5 million deaths per year. BC is the most common cancer in Bangladeshi women and is predicted to be an increasingly important cause of morbidity and mortality in the next 20 years. To date, no population-based cancer registries or a central registry with comprehensive national cancer data is available. For Bangladeshi women with human epidermal growth factor receptor (HER2), estrogen receptor (ER) and progesterone receptor (PR) negative patients (~25%) have no effective targeted therapies. In addition, it is currently not known whether these patients carry mutations in either BRCA1 or BRCA2 genes as there is no genetic screening system available in Bangladesh. Mutations in other genes such as TP53, PTEN and CASP8 are also found in BC patients worldwide but their penetrance in Bangladeshi populations remains unknown. The major objective of this research is to determine the genetic landscape of Bangladeshi BC patients to inform better diagnosis, prognosis, treatment and counselling.Current Research Collaborations: Dr. Klaus Pors, Institute of Cancer Therapeutics (University of Bradford)Dr. Steve Shnyder, Institute of Cancer Therapeutics (University of BradfordProf. Paul Loadman, Institute of Cancer Therapeutics (University of Bradford)Prof. Tim Palmer, School of Pharmacy (University of Bradford) Prof. Colin Wright, School of Pharmacy (University of Bradford)Prof. Richard Trembath (Queen Marry London, UK)Prof. N.W. Morrell (Cambridge, UK)Prof. Ian Eperon (Leicester, UK)Prof. Lan Zhao and Prof. Martin Wilkins (Imperial College, UK)Prof.. Matt Walter (Washington University, USA)Dr. Yi-Tao, (Rochester University, USA)Dr. Christina Bunfii, (IRCCS, Milano, Italy)Dr. Hao Jiang, (University of Alabama at Birmingham, USA)
Research collaborators
Name | Company | Country | Type | Role | Theme | Description |
---|---|---|---|---|---|---|
University of Alabama at Birmingham | US | EXTERNAL | ||||
IRCCS, Milano | IT | EXTERNAL | ||||
Rochester University | US | EXTERNAL | ||||
Washington University | US | EXTERNAL | ||||
University of Cambridge | GB | EXTERNAL | ||||
King's College London | GB | EXTERNAL | ||||
University of Leicester | GB | EXTERNAL |
Contract researchers
Name | Role | Project | Duration | Funding body |
---|---|---|---|---|
Masters (Research) Student | Identification of Novel Factors that Regulate Tissue Specific Alternative Splicing | |||
Masters (Research) Student | Functional consequences of BMPR2 mutations in pulmonary arterial hypertension | |||
Other | Resolution of pulmonary arterial hypertension by novel small molecule agents | |||
Other | Pulmonary Hypertension | |||
PhD Student | Prostanoid-mediated inhibition of IL-6 trans-signalling in pulmonary arterial hypertension; a role for Epac1-mediated induction of "suppressor of cytokine signalling 3" (SOCS3) | |||
PhD Student | Resolution of pulmonary arterial hypertension (PAH) by modulating BMP and TGFb signalling pathways | |||
PhD Student | Pulmonary Hypertension | |||
PhD Student | Resolution of PAH by natural products | |||
PhD Student | Pulmonary Hypertension | |||
PhD Student | Pulmonary Hypertension | |||
Senior Postdoctoral Researcher | Development of diagnostic biomarker for pulmonary arterial hypertension (PAH) | |||
Postdoctoral Researcher | Determination of the efficacy of natural products in pulmonary artrial hjypertension |
Professional activities
Information about education, employment and areas of particular interest for Dr. Talat Nasim is as follows:
Employment
- King’s College London - Visiting Senior Research Fellow in the year 2013 (specified as 01/01/2013)
- Agriculture and Socio-economic Advancements (CHASA), Bangladesh - Founder and Chief Adviser (Honorary) in the year 2008 (specified as 01/01/2008)
- King’s College London - Senior Research Fellow in the year 2008 (specified as 01/01/2008)
- King’s College London - Research Associate in the year 2006 (specified as 01/01/2006)
- University of Leicester - Research Associate in the year 2006 (specified as 01/01/2006)
- University of Leicester - Research Associate in the year 2000 (specified as 01/01/2000)
- University of Geneva - Post-graduate Research Fellow in the year 1994 (specified as 01/01/1994)
Education
- University of Manchester - PhD
Publications
There are 23 publications involving or that are attributed to Dr. Talat Nasim. They are listed as:
- article (1)
- editorial (2)
- peer reviewed journal (19)
- reviews (1)
Article
Title | Year | Publication name | Journal | Volume | Pages | Authors | Editors | ISSN | Publisher | DOI | Location |
---|---|---|---|---|---|---|---|---|---|---|---|
Effectiveness of herbal plants in preventing coronavirus | 2020 | Nasim MT | http://m.thedailynewnation.com/news/251559/effectiveness-of-herbal-plants-in-preventing-virus |
Editorial
Title | Year | Publication name | Journal | Volume | Pages | Authors | Editors | ISSN | Publisher | DOI | Location |
---|---|---|---|---|---|---|---|---|---|---|---|
Coronavirus- our duties to prevent and halt the outbreak | 2020 | Nasim, MT | The Daily New Nation | http://thedailynewnation.com/news/250850/coronavirus--our-duties-to-prevent-and-halt-the-outbreak.html | |||||||
Coronavirus diseases: prevention and treatment | 2020 | Nasim, MT | The Lalmonirhat Barta |
Peer Reviewed Journal
Title | Year | Publication name | Journal | Volume | Pages | Authors | Editors | ISSN | Publisher | DOI | Location |
---|---|---|---|---|---|---|---|---|---|---|---|
Stoichiometric imbalance in the receptor complex contributes to dysfunctional BMPR-II mediated signalling in pulmonary arterial hypertension | 2008 | Nasim, Md. Talat; Ghouri, A.; Patel, B.; James, V.; Rudarakanchana, N.; Morrell, N.W.; Trembath, R.C. | |||||||||
Molecular genetic characterization of SMAD signaling molecules in pulmonary arterial hypertension | 2011 | Nasim, Md. Talat; Ogo, T.; Ahmed, Mohammed I.; Randall, R.; Chowdhury, H.M.; Snape, K.M.; Bradshaw, T.Y.; Southgate, L.; Lee, G.J.; Jackson, I.; Lord, G.M.; Gibbs, J.S.; Wilkins, M.R.; Ohta-Ogo, K.; Nakamura, K.; Girerd, B.; Coulet, F.; Soubrier, F.; Humbert, M.; Morrell, N.W.; Trembath, R.C.; Machado, R.D. | |||||||||
BMPR-II deficiency elicits pro-proliferative and anti-apoptotic responses through the activation of TGFbeta-TAK1-MAPK pathways in PAH | 2012 | Nasim, Md. Talat; Ogo, T.; Chowdhury, H.M.; Zhao, L.; Chen, C-n.; Rhodes, C.; Trembath, R.C. | |||||||||
Recurrent mutations in the U2AF1 splicing factor in myelodysplastic syndromes | 2012 | Graubert, T.A.; Shen, D.; Ding, L.; Okeyo-Owuor, T.; Lunn, C.L.; Shao, J.; Krysiak, K.; Harris, C.C.; Koboldt, D.C.; Larson, D.E.; McLellan, M.D.; Dooling, D.J.; Abbott, R.M.; Fulton, R.S.; Schmidt, H.; Kalicki-Veizer, J.; O'Laughlin, M.; Grillot, M.; Baty, J.; Heath, S.; Frater, J.L.; Nasim, Md. Talat; Link, D.C.; Tomasson, M.H.; Westervelt, P.; DiPersio, J.F.; Mardis, E.R.; Ley, T.J.; Wilson, R.K.; Walter, M.J. | |||||||||
Proteomics of tissue factor silencing in cardiomyocytic cells reveals a new role for this coagulation factor in splicing machinery control | 2015 | Lento, S.; Brioschi, M.; Barcella, S.; Nasim, Md. Talat; Ghilardi, S.; Barbieri, S.S.; Tremoli, E.; Banfi, C. | |||||||||
Inhibition of Overactive Transforming Growth Factor–β Signaling by Prostacyclin Analogs in Pulmonary Arterial Hypertension | 2013 | Ogo, T.; Chowdhury, H.M.; Yang, J.; Long, T.; Li, X.; Torres Cleuven, Y.N.; Morrell, N.W.; Schermuly, R.T.; Trembath, R.C.; Nasim, Md. Talat | |||||||||
Pulmonary arterial hypertension: molecular genetic basis and emerging treatments | 2012 | Siddiqui, M.A.; Ogo, T.; Nasim, Md. Talat | |||||||||
Data for proteomic analysis of murine cardiomyocytic HL1 cells treated with siRNA against tissue factor | 2015 | Brioschi, M.; Lento, S.; Barcella, S.; Nasim, Md. Talat; Tremoli, E.; Banfi, C. | |||||||||
AKAP95 regulates splicing through scaffolding RNAs and RNA processing factors | 2016 | Hu, J.; Khodadadi-Jamayran, A.; Mao, M.; Shah, K.; Yang, Z.; Nasim, Md. Talat; Wang, Z.; Jiang, H. | |||||||||
Aminoglycoside-mediated promotion of translation readthrough occurs through a non-stochastic mechanism that competes with translation termination | 2017 | Chowdhury, H.M.; Siddiqui, M.A.; Kanneganti, S.; Sharmin, N.; Chowdhury, M.W.; Nasim, Md. Talat | |||||||||
Aminoglycoside-mediated promotion of translation readthrough occurs through a non-stochastic mechanism that competes with translation termination | 2018 | Human Molecular Genetics | 27 | 373 - 384 | Chowdhury H.;Siddiqui M.;Kanneganti S.;Sharmin N.;Chowdhury M.;Nasim M. | 0964-6906 | 10.1093/hmg/ddx409 | ||||
BMPRII deficiency impairs apoptosis via the BMPRII-ALK1-BclX-mediated pathway in pulmonary arterial hypertension (PAH) | 2019 | Chowdhury, H.M.; Sharmin, N.; Yuzbasioglu Baran, M.; Long, L.; Morrell, N.W.; Trembath, R.C.; Nasim, Md. Talat | |||||||||
BMPRII deficiency impairs apoptosis via the BMPRII-ALK1-BclX-mediated pathway in pulmonary arterial hypertension | 2019 | Human Molecular Genetics | 28 | 2161 - 2173 | Chowdhury H.;Sharmin N.;Yuzbasioglu Baran M.;Long L.;Morrell N.;Trembath R.;Nasim M. | 0964-6906 | 10.1093/hmg/ddz047 | ||||
A dual-light reporter system to determine the efficiency of protein-protein interactions in mammalian cells. | 2005 | Nucleic Acids Research | 33 | Nasim MT;Trembath RC; | 1362-4962 | 10.1093/nar/gni066 | |||||
The activity of a single-stranded promoter of plasmid ColIb-P9 depends on its secondary structure. | 2004 | Molecular Microbiology | 53 | Nasim MT;Eperon IC;Wilkins BM;Brammar WJ; | 0950-382X | 10.1111/j.1365-2958.2004.04114.x | |||||
HnRNP G and Tra2beta: opposite effects on splicing matched by antagonism in RNA binding. | 2003 | Human Molecular Genetics | 12 | Nasim MT;Chernova TK;Chowdhury HM;Yue BG;Eperon IC; | 0964-6906 | 10.1093/hmg/ddg136 | |||||
A double reporter assay for detecting changes in the ratio of spliced and unspliced mRNA in mammalian cells. | 2002 | Nucleic Acids Research | 30 | Nasim MT;Chowdhury HM;Eperon IC; | 1362-4962 | 10.1093/nar/gnf108 | |||||
Eukaryotic selenocysteine incorporation follows a nonprocessive mechanism that competes with translational termination. | 2000 | Journal of Biological Chemistry | 275 | Nasim MT;Jaenecke S;Belduz A;Kollmus H;Flohé L;McCarthy JE; | 0021-9258 | 10.1074/jbc.275.20.14846 | |||||
Resolution of coronavirus disease 2019 (COVID-19). | 2020 | Expert Review of Anti-Infective Therapy | online | Habas K;Nganwuchu C;Shahzad F;Gopalan R;Haque M;Rahman S;Majumder AA;Nasim T; | 1744-8336 | 10.1080/14787210.2020.1797487 |
Reviews
Title | Year | Publication name | Journal | Volume | Pages | Authors | Editors | ISSN | Publisher | DOI | Location |
---|---|---|---|---|---|---|---|---|---|---|---|
Targeting SOCS Proteins to Control JAK-STAT Signalling in Disease | 2019 | Trends in Pharmacological Sciences | 40 | 298 - 308 | Durham G.;Williams J.;Nasim M.;Palmer T. | 0165-6147 | 10.1016/j.tips.2019.03.001 |