Scientist, educator, mentor, and innovator. 

I am currently as Assistant Teaching Professor at CMU-Q, primarily teaching courses in Molecular Biology and Genetics. After graduating with an MSc from King’s College London and a PhD from the University of Leeds, I focused my scientific career on improving our understanding of human diseases, including cardiovascular disease, cancer, rheumatoid arthritis and Type 2 Diabetes. Prior to joining CMU-Q, I served at Weill Cornell Medicine – Qatar for over a decade, where I led studies in transgenic mice supported by a toolkit of CRISPR/Cas9 gene-editing, molecular biology, cell biology, and metabolic assays to uncover mechanisms that promote pathological changes in metabolic disorders and cancer. I also have over 10 years’ experience in higher education, including in teaching genetics and molecular biology in the UK and Qatar, facilitating problem-based learning sessions and journal clubs at WCM-Q, and mentoring junior scientists on research projects. Over 2 dozen mentees have honed their research skills under my guidance, and I am proud of their success as physicians, graduate students, and postdoctoral fellows. I also have a strong interest in research innovation and commercialization, having submitted an invention disclosure describing a novel strategy to treat Type 2 Diabetes. My research program at CMU-Q is focused on understanding the biological mechanims of mammalian aging, and it utilises cellular, molecular, genetic, and pharmacological tools to gain insights into this fundamental process. I am also passionate about promoting equality, diversity, and inclusivity, and my efforts to empower women in science and volunteering work with Qatar Foundation’s Ability Friendly program exemplify this commitment.  

Doctor of Philosophy (PhD), University of Leeds (2010)

Master of Science (MSc), King’s College London (2005)

Research: Mammalian aging; metabolic disorders; molecular biology; genetics; pharmacology; DAMP signaling; immunology; inflammation.

Teaching: Experimental techniques in genetics and molecular biology; pharmacogenetics; genetics. 

A fundamental question in human biology is why and how do we age? What are the underlying biological mechanisms of aging and is it possible to ‘slow down’ the aging process to potentially increase health span, lifespan, or both. Leonard Hayflick’s seminal work lay the foundation for aging research and made it common knowledge that cells have a limited capacity to proliferate. He discovered that cells stopped proliferating after approximately 50 population-doublings (Hayflick limit) and became aged (aka senescent) (they couldn’t proliferate anymore!). Scientists now know that this senescent phenotype occurs because telomeres shorten after each
round of cell division and once the critical limit is reached, the cell becomes senescent (Nobel Prize, 2009). Importantly, scientists also discovered that cells show signs of premature or accelerated aging in conditions like obesity, type 2 diabetes, and cancer (Raffaella Di Micco et al., Nature Reviews, 2020). This is due to exposure to cellular stress factors like DNA damage, mutations, mitochondrial DNA damage, and oxidative stress. Prematurely aged cells also show signs of inflammation, and they secrete many pro-inflammatory cytokines and chemokines (Audrey Lasry et al., Trends in Immunology, 2015). This is an important finding because scientists are now working on the idea that if we can find strategies to reduce inflammation in prematurely aged cells, then this may reverse the premature senescence phenotype and be potentially therapeutic in conditions like diabetes and cancer.   

Research program: Danger-Associated Molecular Patterns (DAMPs) are key components of the immune system and examples include molecules like ATP and ADP, which are secreted by stressed (dying, infected etc.) cells to request help from the immune system. DAMPs signal to the immune system via specific DAMP receptors (P2X and P2Y receptors, for example). As a scientist at Weill Cornell Medicine – Qatar (WCM-Q), I was awarded 2 Undergraduate Research Experience Program (UREP) grants by QNRF. My students and I discovered and published that prematurely aged preadipocytes and cancer cells expressed very high levels of DAMP receptors. These DAMP receptors, when activated by DAMPs, increased the secretion of interleukin-6 – a potent pro-inflammatory cytokine (Yasser
Majeed et al., British Journal of Pharmacology, 2022). At CMU-Q, my research program will build on this discovery. We will identify the pro-inflammatory DAMP receptors at the molecular level, then test the anti-inflammatory potential of inhibitors targeting these receptors to potentially discover novel pharmacological tools that may reverse inflammation in prematurely senescent cells in the context of diabetes and cancer.  

Methodology: The research program will develop in vitro cellular models of premature senescence, then study their phenotype using techniques like fluorescence microscopy, qPCR, cytokine ELISA, metabolic assays, pharmacology, and cell growth assays. Omics approaches like RNA-sequencing may also be used.  

Collaborations: There will be opportunities to interact and discuss science with collaborators, including scientists like Dr. Rosalyn Abbott (CMU) and Professor Samuel Fountain (University of East Anglia, UK).   

Scientific skills development: Scientific writing; hands-on technical skills; critical thinking; troubleshooting; data analysis and interpretation; statistics; manuscript preparation; oral presentations. 

Literature to read:  

(1) Yasser Majeed et al., British Journal of Pharmacology, 2022. 

(2) Raffaella Di Micco et al., Nature Reviews, 2020. 

(3) Audrey Lasry et al., Trends in Immunology, 2015.    

Mammalian aging; metabolic disorders; molecular biology; genetics; pharmacology; DAMP signaling; immunology; inflammation.

https://scholar.google.com/citations?user=_VnEj3gAAAAJ&hl=en

1. STAT1-and NFAT-independent amplification of purinoceptor function integrates cellular senescence with interleukin-6 production in preadipocytes. Yasser Majeed, Aisha Y. Madani, Ahmed I. Altamimi, Raphael Courjaret, Muneera Vakayil, Samuel J. Fountain, Khaled Machaca, Nayef A. Mazloum. British Journal of Pharmacology, 2023. (Outcome of QNRF grant UREP25-026-3-005 awarded to Yasser Majeed). 

2.SIRT1 promotes lipid metabolism and mitochondrial biogenesis in adipocytes and coordinates adipogenesis by targeting key enzymatic pathways. Yasser Majeed, Najeeb Halabi, Aisha Y. Madani, Rudolf Engelke, Aditya M. Bhagwat, Houari Abdesselem, Maha V. Agha, Muneera Vakayil, Raphael Courjaret, Neha Goswami, Hisham Ben Hamidane, Mohamed A. Elrayess, Arash Rafii, Johannes Graumann, Frank Schmidt and Nayef A. Mazloum. Scientific Reports, 2021 April 14;11(1):8177 (Outcome of QNRF grants NPRP8-059-1-009, NPRP10-1-2051-60010, and GSRA4-1-0330-17010). 

3.Signal transducer and activator of transcription 3 (STAT3) suppresses STAT1/ interferon signaling pathway and inflammation in senescent preadipocytes. Aisha Y. Madani, Yasser Majeed, Houari B. Abdesselem, Maha V. Agha,Muneera Vakayil, Nour K. Alsukhun, Najeeb M. Halabi, Pankaj Kumar, Shahina Hayat, Mohamed A. Elrayess, Arash Rafii, Karsten Suhre, Nayef A. Mazloum. Antioxidants, 2021 February 23; 10(2), 334 (Outcome of QNRF grants NPRP10-1-2051-60010 and GSRA4-1-0330- 17010). 

4. Metabolic profiling of pre-gestational and gestational diabetes mellitus identifies novel predictors of pre-term delivery. Ilhame Diboun, Manjunath Ramanjaneya, Yasser Majeed, Lina Ahmed, Mohammed Bashir, Alexandra E Butler, Abdul Badi Abou- Samra, Stephen L Atkin, Nayef A Mazloum, Mohamed A Elrayess. Journal of Translational Medicine, 2020 September 24; 18(1):366 (Outcome of QNRF grant NPRP10-1-2051-60010). 

5.Potent and PPARα-independent anti-proliferative action of the hypolipidemic drug fenofibrate in VEGF-dependent angiosarcomas in vitro. Yasser Majeed*, Rohit Upadhyay, Sara Alhousseiny, Tarek Taha, Adham Musthak, Yanal Shaheen, Mohtashim Jameel, Chris R Triggle, Hong Ding*. Scientific Reports, 2019 April 19;9(1):6316 (*, corresponding author) (Outcome of QNRF grant NPRP6-42 8-3-113). 

6.Treatment with a Combination of Metformin and 2-Deoxyglucose Upregulates Thrombospondin-1 in Microvascular Endothelial Cells: Implications for Anti- Angiogenic Cancer Therapy. Samson Mathews Samuel, Noothan J Satheesh, SuparnaGhosh, Dietrich Busselberg, Yasser Majeed, Hong Ding and Chris R. Triggle. Cancers (Basel), 2019 Nov 6;11(11) (Outcome of QNRF grant NPRP 04-910-3-244). 

7.Metformin Represses Glucose Starvation Induced Autophagic Response in Microvascular Endothelial Cells and Promotes Cell Death. Samson Mathews Samuel, Suparna Ghosh, Yasser Majeed, Gnanapragasam Arunachalam, Mohamed M Emara, Hong Ding, Chris R Triggle. Biochemical Pharmacology, 2017 May; 132:118- 132 (Outcome of QNRF grant NPRP 04-910-3-244). 

8.Piezo1 integration of vasculature architecture with physiological force. Li J, Hou B, Tumova S, Muraki K, Bruns A, Ludlow MJ, Sedo A, Hyman AJ, McKeown L, Young RS, Yuldasheva NY, Majeed Y, Wilson LA, Rode B, Bailey MA, Kim HR, Fu Z, Carter DA, Bilton J, Imrie H, Ajuh P, Dear TN, Cubbon RM, Kearney MT, Prasad RK, Evans PC, Ainscough JF, Beech DJ. Nature, 2014 Nov; 515(7526):279-282. 

9.Inhibition of endothelial cell Ca2+ entry and Transient Receptor Potential channels by Sigma-1 receptor ligands. Amer MS, McKeown L, Tumova S, Liu R, Seymour VA, Wilson LA, NaylorJ, Greenhalgh K, Hou B, Majeed Y, TurnerP, Sedo A, O’Regan DJ, Li J, Bon RS, Porter KE, Beech DJ. British Journal of Pharmacology, 2013 Mar; 168(6): 1445-55. 

10. Pregnenolone sulphate-independent inhibition of TRPM3 channels by progesterone. Majeed, Y., Tumova, S., Green, B.L., Seymour V.A.L., Woods, D.M., Agarwal, A.K., Naylor, J., Jiang, S., Picton, H.M., Porter, K.E., O’Regan, D.J., Muraki, K., Fishwick, C.W.G., Beech, D.J. Cell Calcium, 2012 Jan; 51(1):1-11. 

11. Rapid and contrasting effects of rosiglitazone on TRPM3 and TRPC5 channels. Majeed, Y., Bahnasi, Y., Seymour, V.A.L., Wilson, L.A., Milligan, C.J., Agarwal, A.K., Sukumar, P., Naylor, J., Beech, D.J. Molecular Pharmacology, 2011 Jun; 79(6):1023- 30. 

12. TRPC1 transcript variants, inefficient nonsense-mediated decay and low up- frameshift-1 in vascular smooth muscle cells. Alexandra Dedman, Yasser Majeed, Sarka Tumova, Fanning Zeng, Bhaskar Kumar, Christopher Munsch, Alan Bateson, Jurgen Wittmann, Hans-Martin Jack, Karen Porter, David J Beech. BMC Molecular Biology, 2011 July 12; 12:30. 

13. GVI phospholipase A2 role in the stimulatory effect of sphingosine-1-phosphate on TRPC5 cationic channels. Al-Shawaf, E., Tumova, S., Naylor, J., Majeed, Y., Li, J., Beech, D.J. Cell Calcium, 2011 October; 50(4):343-50. 

14. Orai1 and CRAC channel dependence of VEGF-activated Ca2+ entry and endothelial tube formation. Li, J., Cubbon, R.M., Wilson, L.A., Amer, M.S., McKeown, L., Hou, B., Majeed, Y., Tumova, S., Seymour, V.A.L., Taylor, H., Stacey, M., O’Regan, D., Foster, R., Porter, K.E., Kearney, M.T., Beech, D.J. Circulation Research, 2011 May; 108(10):1190-8. 

15. Stereo-selective inhibition of TRPC5 channels by neuroactive steroids. Yasser Majeed, Mohamed Amer, Anil Agarwal, Lynn McKeown, Karen Porter, David O’Regan, Jacqueline Naylor, Colin Fishwick, Katsuhiko Muraki, David J Beech. British Journal of Pharmacology, 2011 Apr; 162(7):1509-20. 

16. Cis-isomerism and other chemical requirements of steroidal agonists and partial agonists acting at TRPM3 channels. Yasser Majeed, Anil Agarwal, Jacqueline Naylor, Victoria AL Seymour, Shan Jiang, Katsuhiko Muraki, Colin Fishwick, David J Beech. British Journal of Pharmacology, 2010 Sep; 161(2):430-41. 

17. TRPM3 channel stimulated by pregnenolone sulphate in synovial fibroblasts and negatively coupled to hyaluronan. Coziana Ciurtin†, Yasser Majeed†, Jacqueline Naylor, Piruthivi Sukumar, Anne English, Paul Emery & David J Beech. BMC Musculoskeletal Disorders, 2010 June; 11:111 (†, equal contributors). 

18. Pregnenolone-sulphate and cholesterol-regulated TRPM3 channels coupled to vascular smooth muscle secretion and contraction. Jacqueline Naylor, Jing Li, Carol J Milligan, Fanning Zeng, Piruthivi Sukumar, Bing Hou, Alicia Sedo, Nadira Yuldasheva, Yasser Majeed, Dhananjay Beri, Shan Jiang, Victoria AL Seymour, Lynn Mckeown, Bhaskar Kumar, Christian Harteneck, DavidO’Reagan, Stephen B Wheatcroft, Mark T Kearney, Clare Jones, Karen E Porter & David J Beech. Circulation Research, 2010 May 14; 106(9):1507-15. 

19. Robotic multi-well planar patch-clamp for native and primary mammalian cells. Carol J Milligan, Jing Li, Piruthivi Sukumar, Yasser Majeed, Mark Dallas, Anne English, Paul Emery, Karen E Porter, Andrew M Smith, Ian McFadzean, Dayne Beccano-Kelly, Yahya Bahnasi, Alex Cheong, Jacqueline Naylor, Fanning Zeng, Xing Liu, Nikita Gamper, Lin-Hua Jiang, Hugh A Pearson, Chris Peers, Brian Robertson and David J Beech. Nature Protocols, 2009; 4(2): 244-55. 

20. TRPC channel activation by extracellular thioredoxin. Xu SZ, Sukumar P, Zeng F, Li J, Jairaman A, English A, Naylor J, Ciurtin C, Majeed Y, Milligan CJ, Bahnasi YM, Al- Shawaf E, Porter KE, Jiang LH, Emery P, Sivaprasadarao A, Beech DJ. Nature, 2008 Jan 3; 451 (7174): 69-72. 

Extramural Grants to support undergraduate research capacity-building programs. 

Lead Principal Investigator (LPI) – Undergraduate Research Experience Program (UREP) Grant – UREP28-048-3-017 (2021).
Funding agency: Qatar National Research Fund. Project: Regulation of proinflammatory cytokines and chemokines by the mechanosensitive protein Piezo1 in DNA-damaged preadipocytes. 

Lead Principal Investigator (LPI) – Undergraduate Research Experience Program (UREP) Grant – UREP25-026-3-005 (2019).
Funding agency: Qatar National Research Fund. Project: Role of the endoplasmic reticulum (ER) protein TMEM38B in promoting senescence, inflammation, and adipose dysfunction in obesity.  

3^rd place, Best Representative Image of an Outcome 6 (BRIO6) competition 2022, QNRF 

1^st place, Poster presentation, WCM-Q Research Retreat 2019 

2^nd place, Poster presentation, WCM-Q Research Retreat 2018