Results 31 to 40 of about 24,552 (280)

The Role of BTK Inhibition in the Treatment of Chronic Lymphocytic Leukemia: A Clinical View

open access: yesJournal of Experimental Pharmacology, 2021
Francesco Paolo Tambaro,1 Danilo De Novellis,1,2 William G Wierda3 1Unità Operativa di Trapianto di Midollo Osseo e Servizio Trasfusionale, Azienda Ospedaliera di Rilievo Nazionale Santobono-Pausilipon, Napoli, Italy; 2Department of Precision Medicine ...
Tambaro FP, De Novellis D, Wierda WG
doaj  

Effective, safe, and sustained correction of murine XLA using a UCOE-BTK promoter-based lentiviral vector

open access: yesMolecular Therapy: Methods & Clinical Development, 2021
X-linked agammaglobulinemia (XLA) is an immune disorder caused by mutations in Bruton’s tyrosine kinase (BTK). BTK is expressed in B and myeloid cells, and its deficiency results in a lack of mature B cells and protective antibodies.
Brenda J. Seymour   +12 more
doaj   +1 more source

Btk inhibitors in atherosclerosis [PDF]

open access: yesBlood, 2018
In this issue of Blood, Busygina et al provide provocative evidence that there is a potential role for Bruton tyrosine kinase (Btk) inhibitors in inhibiting platelet aggregation specifically at the site of unstable atherosclerotic plaques ...
openaire   +2 more sources

Amplifying Btk's Signal [PDF]

open access: yesImmunity, 2003
The Tec kinase Btk is an important regulator of antigen receptor activation of phospholipase C-gamma (PLC-gamma). Data from Carpenter and colleagues (Saito et al., this issue of Immunity) now suggest that Btk also activates phosphatidylinositol-4-phosphate 5-kinase (PIP5K), thereby stimulating a positive feedback loop that generates PI(4,5)P2, the ...
openaire   +2 more sources

Inverting the BTK-BCL2 order [PDF]

open access: yesBlood, 2020
In this issue of Blood, Lin et al report the first long-term follow-up data showing that Bruton tyrosine kinase inhibitors (BTKi's) are effective in chronic lymphocytic leukemia (CLL) after previous progression on venetoclax.
openaire   +2 more sources

Bruton’s tyrosine kinase regulates gut immune homeostasis through attenuating Th1 response

open access: yesCell Death and Disease, 2021
Inflammatory bowel disease (IBD) is driven by multiple genetic and environmental risk factors. Patients with mutations in Bruton’s tyrosine kinase (BTK) is known to manifest high prevalence of intestinal disorders including IBD. Although BTK mediates the
Di Guan   +4 more
doaj   +1 more source

Structural Complementarity of Bruton’s Tyrosine Kinase and Its Inhibitors for Implication in B-Cell Malignancies and Autoimmune Diseases

open access: yesPharmaceuticals, 2023
Bruton’s tyrosine kinase (BTK) is a critical component in B-cell receptor (BCR) signaling and is also expressed in haematogenic and innate immune cells. Inhibition of BTK hyperactivity is implicated in B-cell malignancies and autoimmune diseases.
Asim Najmi   +8 more
doaj   +1 more source

Bruton’s Tyrosine Kinase and Its Isoforms in Cancer

open access: yesFrontiers in Cell and Developmental Biology, 2021
Bruton’s tyrosine kinase (BTK) is a soluble tyrosine kinase with central roles in the development, maturation, and signaling of B cells. BTK has been found to regulate cell proliferation, survival, and migration in various B-cell malignancies.
Xianhui Wang   +3 more
doaj   +1 more source

Targeting Bruton’s Tyrosine Kinase in Inflammatory and Autoimmune Pathologies

open access: yesFrontiers in Cell and Developmental Biology, 2021
Bruton’s tyrosine kinase (BTK) was discovered due to its importance in B cell development, and it has a critical role in signal transduction downstream of the B cell receptor (BCR).
Stefan F. H. Neys   +2 more
doaj   +1 more source

A Comprehensive Review of Small-Molecule Inhibitors Targeting Bruton Tyrosine Kinase: Synthetic Approaches and Clinical Applications

open access: yesMolecules, 2023
Bruton tyrosine kinase (BTK) is an essential enzyme in the signaling pathway of the B-cell receptor (BCR) and is vital for the growth and activation of B-cells.
Qi Zhang   +3 more
doaj   +1 more source

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