Rashi Singhal, PhD

Yatrik Shah Lab

7703 Med Sci II
Ann Arbor MI 48109-5622

734-615-5041

Areas of Interest

I have a longstanding interest in studies directed at understanding basic mechanisms regulating immune responses in inflammatory diseases and Cancer. As a Post doctoral researcher in Shah Lab I am studying metabolic mechanisms regulating immune-suppressive functions of myeloid derived suppressor cells in colon cancer.

Honors & Awards

  • 2009 - 2011 Scholarship, National Merit Scholarship Program for Master of Science
  • 2012 - 2018 Scholarship, Department of biotechnology, Govt. of India
  • 2011 Qualified Graduate Aptitude Test Engineering (GATE) in Biotechnology with 97.35 percentile
  • 2013 Qualified CSIR National Eligibility Test holding 27th Rank
  • 2016 Best Poster Presentation Award, 3rd AIST International Imaging WS Tsukuba, Japan
  • 2017 “Torrent Young Investigator Award” for Oral presentation, Cardiovascular Research Convergence, THSTI, Faridabad, India
  • 2017 “Best Poster award”, Cardiovascular Research Convergence, THSTI, Faridabad,
  • 2018 “Winner Prize”, Science Communication competition, Science Day, RCB, Faridabad, India
  • 2018 “Reach-the World travel Grant”, (ISTH-SSC) meeting in Dublin, Ireland
  • 2018 “Best Prize”, Poster Competition in RCB OPEN DAY- Outreach program under India International Science Festival held on 24th September, 2018
  • 2018 “Best Prize”, Poster Competition in Immunocon, Indian Immunology Society Conference held at THSTI, Faridabad, India

Credentials

  • PhD, Biotechnology, Regional Centre for Biotechnology-Faridabad India

Published Articles or Reviews

  • Singhal R, Shah YM. (2020) Hypoxia and HIFs as metabolic and inflammatory gatekeepers in intestine. JBC.
  • Singhal R, Mitta SR, Olive KP, Lyssiotis C and Shah YM. (2019) Hypoxia inducible factor-2α increases sensitivity of colon cancer cells towards oxidative cell death. Biorxiv. doi: https://doi.org/10.1101/823997
  • Singhal R, Rathore DK, Bhakuni T, Seth T and Guchhait P. (2019) Absence of non-classical monocytes in haemolytic patients: free Hb and NO mediated mechanisms. J Immunol Res.
  • Bhakuni T, Singhal R, Annarapu G, Sharma A, Mahapatra M, Saxena R, Guchhait P. (2019) Unique case of autoantibody mediated inactivation of ADAMTS13 in an Indian TTP patient. Blood cells, Molecules and Diseases. 77: 29-33.
  • Singhal R, Chawla S, Batra H, Gupta S, Ojha A, Rathore DK, Seth T and Guchhait P. (2018). Engulfment of Hb-activated platelets differentiates monocytes into pro-inflammatory macrophages in PNH patients. Eur. J. Immunol. doi: 10.1002/eji.201747449.
  • Singhal R, Chawla S, Rathore DK, Bhasym A, Annarapu GK, Sharma V, Seth T, and Guchhait P. (2017) Development of pro-inflammatory phenotype in monocytes after engulfing Hb-activated platelets in hemolytic disorders. Clin. Immunol. 175: 133-142.
  • Ojha A, Nandi D, Batra H, Singhal R, Annarapu GK, Bhattacharyya S, Seth T, Dar L, Medigeshi GR, Vrati S, Vikram NK and Guchhait P. (2017) Platelet activation determines the severity of thrombocytopenia in dengue infection. Sci. Rep. 7:41697. doi: 10.1038/srep41697
  • Annarapu GK*, Singhal R*, Gupta A, Chawla S, Batra H, Seth T, Guchhait P.
    (2016) HbS binding to GP1bα activates platelets in sickle cell disease. Plos One 11(12): e0167899. (* Equal first author)
  • Annarapu GK*, Singhal R*, Peng Y, Guchhait P. (2016) Inhibition of Hb binding to GP1bα abrogates Hb-mediated thrombus formation on immobilized VWF and collagen under physiological shear stress. Plos One, 11(4): e0154276. (* Equal first author)
  • Singhal R, Annarapu GK, Pandey A, Chawla S, Ojha A, Gupta A, Cruz MA, SethT, Guchhait P. (2015) Hemoglobin interaction with GP1bα induces platelet activation and apoptosis: a novel mechanism associated with intravascular hemolysis. Haematologica, 100: 1526-33
  • Annarapu GK, Singhal R, Chawla S, Ojha A, Guchhait P. (2016) Hemoglobin Mediated Regulation of Platelet Functions. J Hematol Transfus 4(3): 1052.
  • Batra H, Chawla S, Singhal R, Annarapu GK and Guchhait P. (2016) Cell free hemoglobin modulates phenotype and function of immune cells in hemolytic disorders. Austin. Hematol 1(10): 1-6.

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