Results 121 to 130 of about 7,490 (233)

Bruton’s Tyrosine Kinase Inhibition for the Treatment of Rheumatoid Arthritis

open access: yesImmunoTargets and Therapy, 2021
Laura C Arneson,1,* Kristen J Carroll,1,* Eric M Ruderman2 1Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA; 2Department of Medicine, Division of Rheumatology, Northwestern University Feinberg School ...
Arneson LC, Carroll KJ, Ruderman EM
doaj  

DNA methyltransferase inhibitors in hematological malignancies and solid tumors

open access: yesInternational Journal of Cancer, Volume 158, Issue 2, Page 433-461, 15 January 2026.
Abstract Epigenetic modifications such as DNA methylation play a fundamental role in oncogenesis and the progression of neoplasms neoplasias. DNA methyltransferase inhibitors (DNMTi) constitute a family of therapeutic agents that impede the methylation at the 5‐position on cytosine nucleotides, thereby modulating the epigenetic regulation of tumor ...
Valentin Wenger   +3 more
wiley   +1 more source

Profound Sinoatrial Arrest Associated with Ibrutinib

open access: yesCase Reports in Oncological Medicine, 2017
Background. Ibrutinib is a Bruton’s tyrosine kinase (BTK) inhibitor approved for second-line treatment for mantle cell lymphoma (MCL), chronic lymphocytic leukemia (CLL), and Waldenström macroglobulinemia.
Kanupriya Mathur   +3 more
doaj   +1 more source

Regulatory Mechanism of PTP-PEST for IgE Fc Receptor Signaling [PDF]

open access: yes, 2010
連続したくしゃみ、止まらない鼻水などやっかいな症状で悪名の高い所謂「アレルギー」を直接引き起こす細胞は、マスト細胞もしくは好塩基球である。マスト細胞は、IgE 受容体 (FcεR) を介して活性化され、顆粒中に蓄えた炎症物質放出と炎症性サイトカインの合成・放出によりアレルギー性炎症を惹起する。この細胞内シグナル伝達において、種々のタンパク質中のチロシンリン酸化と脱リン酸化制御が重要な働きをしている。我々は、以前、マスト細胞のFcεRシグナルにおける各種チロシン脱リン酸化酵素(PTP ...
片桐 達雄, 鈴木 望美
core   +1 more source

Involvement of Bruton's tyrosine kinase in FcepsilonRI-dependent mast cell degranulation and cytokine production. [PDF]

open access: yes, 1998
We investigated the role of Bruton's tyrosine kinase (Btk) in FcepsilonRI-dependent activation of mouse mast cells, using xid and btk null mutant mice.
Alt, FW   +16 more
core  

Génexpressziós profil vizsgálata a pajzsmirigy hámeredetű tumoraiban = Gene-expression profiles in the thyroid tumors of epithelial origin [PDF]

open access: yes, 2007
A thyroid tumorok kialakulása az epitelialis carcinogenezis többlépcsős modelljeként irható le. Tumor szuppresszor gének, és az onkogének három fő csoportjába tartozó gének (GTP-kötő protein, sejtmagi transzkripciós faktor, tirozin kináz) mutációinak ...
Ember, István   +2 more
core  

Isoform of Bruton's tyrosine kinase (BTK) protein

open access: yes, 2008
The use of compounds is described which are capable of functionally blocking at least one of the genes chosen from the group composed of EphA1, EphA2, EphA8, EphB2, CSF1R, VEGFR2, RAMP2, RAMP3, CLRN1, MAPK4, PIK3C2A, PIK3CG, GSK3alpha, GSK3beta, IRAK3, DAPK1, JAK1, PIM1, TRB3, BTG1, LATS1, LIMK2, MYLK, PAK1, PAK2, CDC2, BTK, PNRC2, NCOA4, NR2C1, TPR ...
LAVITRANO, MARIALUISA   +2 more
openaire   +2 more sources

Novel Bruton's tyrosine kinase inhibitors currently in development.

open access: yesOncoTargets and therapy, 2013
Bruton's tyrosine kinase (Btk) is intimately involved in multiple signal-transduction pathways regulating survival, activation, proliferation, and differentiation of B-lineage lymphoid cells. Btk is overexpressed and constitutively active in several B-lineage lymphoid malignancies.
D’Cruz, Osmond J, Uckun, Fatih M
openaire   +2 more sources

Functional interaction between CD180 Toll-like receptor (TLR) and B cell receptor (BCR) in the biology of Chronic Lymphocytic Leukaemia (CLL) [PDF]

open access: yes, 2017
Chronic Lymphocytic Leukaemia (CLL) is the most common leukaemia in the western world and remains incurable. It is driven by as yet unknown (auto)antigens via the B cell receptor (BCR) and growth, survival and expansion signals it receives from the ...
Rajakaruna, A., Rajakaruna, A.
core  

Division of Analysis of Homeostasis [PDF]

open access: yes, 2007
この論文は国立情報学研究所の学術雑誌公開支援事業により電子化されまし
永井 博弌
core   +1 more source

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