Kasturi Pal

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Kasturi Pal

Assistant Professor of Biology, Ashoka University

Ph.D., University of California Riverside
https://kasturipal.wixsite.com/website kasturi.pal@ashoka.edu.in

Katuri Pal received her bachelor’s degree in Physiology from Presidency College, University of Calcutta and went on to complete her masters from Madurai Kamaraj University. During her PhD training, she worked in the laboratory of Dr. Kathryn Defea at the University of California, Riverside. For her PhD thesis she worked on non-canonical, scaffold driven signaling by G protein coupled receptors (GPCRs). As a part of her PhD training, she was actively involved with teaching undergraduate students of biology. She then joined Dr. Saikat Mukhopadhyay’s laboratory at the University of Texas Southwestern Medical Center, for her postdoctoral training. Here, she worked on the regulation of the Sonic Hedgehog pathway by GPCRs which localized to the primary cilia. She then joined the laboratory of Dr. Velia Fowler, at the Scripps Research Institute, as a Judith Graham Poole postdoctoral fellow to work on the role of cytoskeletal proteins in megakaryocyte to platelet differentiation.

With her interdisciplinary training in both in-vitro and in-vivo aspects of biology, she looks forward to solve challenging biological problems with a holistic approach. The overarching goal of her research is to understand the role of GPCR signaling and intracellular trafficking in hematopoietic systems, by using biochemical and cell biological approaches. The major questions, she look forward to addressing include:

  1. What are the roles of GPCRs in platelet biogenesis?

  2. How are vesicles synthesized and secreted in platelets?

  3. How can platelets be synthesized ex-vivo to meet transfusion requirements of thrombocytopenia patients?

Curious students with an interest in cell biology and signal transduction pathways can contact her with your CV and cover letter. We are always looking for creative and dedicated scientists to join the laboratory.

  1. Pal K, Nowak R, Billington N, Li R, Ghosh A, Sellers J, Fowler V. (2020). Megakaryocyte migration defects due to nonmuscle myosin IIA mutations underly thrombocytopenia in MYH9-Related Disease. Blood. 135(21):1887 1898 https://doi.org/10.1182/blood.2019003064. * Cover image of Blood [May 21st, 2020]
  2. Pal K, Hwang SH, Somatilaka B, Badgandi H, Jackson P, Defea K, Mukhopadhyay S. (2016). Smoothened and β-arrestins cooperate to determine steady state and sonic hedgehog mediated removal of the G-protein coupled receptor Gpr161 from the primary cilium. J Cell Biol. 212(7): 861-75.

  3. Pal K, Nowak R, Billington N, Li, R, Sellers J, Fowler V.  (2019). Non-muscle myosin II A mutations associated with MYH9-related disorders result in coagulopathies due to impaired megakaryocyte migration in bone marrow niches. (Manuscript in press).

  4.  Rivas C, Yee M, Addison K, Lovett M, Pal K, Ledford J, Dussor G, Price T, Vagner J, DeFea K, Boitano S. (2019). Novel proteinase-activated receptor-2 (PAR2) antagonist C391 blocks Alternaria induced human airway epithelial signaling and asthma indicators in murine models. (Manuscript in review in British Journal of Pharmacology)

  5. Smith AS, Pal K, Nowak RB, Demenko A, Da Costa L, Favier R, Pecci A, Fowler V. (2019). MYH9-related disease mutations cause abnormal red blood cell morphology through increased myosin-actin binding at the membrane. Am J Hematol. doi: 10.1002/ajh.25472 [Impact factor: 5.3]

  6.  Nichols H, Yee M, Polley D, Saifeddine M, Pal K, Lee K, Daines M, Wilson E, Boitano S, Hollenberg M, DeFea K. (2018). Protease-activated-Receptor-2-Induced signaling through β-arrestin-2 Mediates Alternaria Serine Protease-induced Asthma. Am J Physiol Lung Cell Mol Physiol. 315(6): L1042-L1057. [Impact factor: 4.092]

  7.  Mukhopadhyay S, Badgandi H, Hwang SH, Somatilaka B, Shimada I, Pal K. (2017). Trafficking to the primary cilium membrane. Mol Biol Cell. 28(2): 233-239. [Impact factor: 3.512].

  8. Pal K, Hwang SH, Somatilaka B, Badgandi H, Jackson P, Defea K, Mukhopadhyay S. (2016). Smoothened and β-arrestins cooperate to determine steady state and sonic hedgehog mediated removal of the G-protein- coupled receptor Gpr161 from the primary cilium. J Cell Biol. 212(7): 861-75. [Impact factor: 8.784]

            *Article in focus by Ben Short-  http://jcb.rupress.org/content/early/2016/03/21/jcb.2127iti3.1

  1. Pal K, Badgandi H, Mukhopadhyay S. (2015). Studying G-protein-coupled receptors: Immunoblotting, immunoprecipitation, phosphorylation, surface labeling, and cross-linking protocols. Methods Cell Biol. 127:303-22. [Impact factor: 1.588]

  2. Pal K, Mukhopadhyay S. (2015). Primary Cilium and sonic hedgehog signaling during neural tube patterning: Role of GPCRs and second messengers. Developmental Neurobiology. 75(4): 337-48. doi: 10.1002/dneu.22193. [Impact factor: 4.423]

  3.  Mittal N, Roberts K, Pal K, Bentolila LA, Fultz E, Minasyan A, Cahill C, Pradhan A, Conner D, Defea K, Evans C, Walwyn W. (2013). Select G-Protein-Coupled Receptors Modulate Agonist-Induced Signaling via a ROCK, LIMK, and β-Arrestin 1 Pathway. Cell Rep. 5(4): 1010-21. [Impact factor: 8.032]

  4. Pal K, Mathur M, Kumar P, DeFea K. (2013). Divergent β-arrestin-dependent signaling events are dependent upon sequences within G-protein-coupled-receptor C-termini. J Biol Chem. 288(5): 3265-74. [Impact factor: 4.106]

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