Inhibition of inositol kinase B controls acute and chronic graft-versus-host disease | Zendy

Govindarajan Thangavelu | Zendy; Jing Du | Zendy; Katelyn Paz | Zendy; Michaël Loschi | Zendy; Michael Zaiken | Zendy; Ryan Flynn | Zendy; Patricia A. Taylor | Zendy; Andrew Kemal Kirchmeier | Zendy; Angela PanoskaltsisMortari | Zendy; Leo Luznik | Zendy; Kelli P. A. MacDonald | Zendy; Geoffrey R. Hill | Zendy; Ivan Maillard | Zendy; David H. Munn | Zendy; Jonathan S. Serody | Zendy; William J. Murphy | Zendy; David B. Miklos | Zendy; Corey Cutler | Zendy; John Koreth | Zendy; Joseph H. Antin | Zendy; Robert J. Soiffer | Zendy; Jerome Ritz | Zendy; Carol Dahlberg | Zendy; Andrew T. Miller | Zendy; Bruce R. Blazar | Zendy

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Inhibition of inositol kinase B controls acute and chronic graft-versus-host disease

Author(s) -

Govindarajan Thangavelu,

Jing Du,

Katelyn Paz,

Michaël Loschi,

Michael Zaiken,

Ryan Flynn,

Patricia A. Taylor,

Andrew Kemal Kirchmeier,

Angela PanoskaltsisMortari,

Leo Luznik,

Kelli P. A. MacDonald,

Geoffrey R. Hill,

Ivan Maillard,

David H. Munn,

Jonathan S. Serody,

William J. Murphy,

David B. Miklos,

Corey Cutler,

John Koreth,

Joseph H. Antin,

Robert J. Soiffer,

Jerome Ritz,

Carol Dahlberg,

Andrew T. Miller,

Bruce R. Blazar

Publication year - 2019

Publication title -

blood

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 5.515

H-Index - 465

eISSN - 1528-0020

pISSN - 0006-4971

DOI - 10.1182/blood.2019000032

Subject(s) - immunology , graft versus host disease , cancer research , t cell , pathogenesis , myeloid leukemia , biology , medicine , microbiology and biotechnology , immune system , stem cell

T-cell activation leads to regulated increases in cytoplasmic calcium through inositol 1,4,5-triphosphate (IP3), a process balanced by phosphorylation and inactivation of IP3 by inositol 1,4,5-trisphosphate 3-kinase B (Itpkb). The investigators demonstrate that inhibition of Itpkb sustains increased intracellular Ca, leads to T-cell apoptosis, and inhibits graft-versus-host disease without impairing graft-versus-leukemia effects.

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