Results 151 to 160 of about 7,128 (244)

Janus Kinases Affect Thrombopoietin Receptor Cell Surface Localization and Stability [PDF]

open access: hybrid, 2005
Yohan Royer   +4 more
openalex   +1 more source

485 In the presence of a PFO, a paradoxical embolism triggered by hormone replacement therapy and Janus Kinase inhibitor

open access: hybrid
Akeem Yusuf   +6 more
openalex   +1 more source

Intramolecular regulation of Janus kinases

open access: yes, 2017
Janus-kinaasit (JAKit) ovat ei-reseptorisia tyrosiinikinaaseja, jotka välittävät yli 60 sytokiinin viestejä soluissa. Nämä viestit säätelevät lukuisia biologisia tapahtumia, kuten immuunijärjestelmän toimintaa, hematopoieesia, aineenvaihduntaa sekä kehitystä.
openaire   +2 more sources

Janus-family tyrosine kinase

open access: yes
Citation: 'Janus-family tyrosine kinase' in the IUPAC Compendium of Chemical Terminology, 5th ed.; International Union of Pure and Applied Chemistry; 2025. Online version 5.0.0, 2025. 10.1351/goldbook.13352 • License: The IUPAC Gold Book is licensed under Creative Commons Attribution-ShareAlike CC BY-SA 4.0 International for individual ...
openaire   +1 more source

Hypomethylating agents in vacuoles, E1 enzyme, X‐linked, autoinflammatory, somatic syndrome (VEXAS): A systematic review

open access: yesBritish Journal of Haematology, EarlyView.
Summary VEXAS syndrome (vacuoles, E1 enzyme, X‐linked, autoinflammatory, somatic) is an X‐linked, systemic, haemato‐inflammatory syndrome caused by somatic mutations in the UBA1 gene. No standardized treatment guidelines exist, but evidence is emerging that treatment with hypomethylating agents (HMAs) can induce improvement of the inflammatory symptoms,
Fieke W. Hoff   +3 more
wiley   +1 more source

Association of myalgias with compounded topical Janus kinase inhibitor use in vitiligo [PDF]

open access: gold, 2020
Shanthi Narla   +4 more
openalex   +1 more source

Janus kinase (JAK) [PDF]

open access: yesScience-Business eXchange, 2014
openaire   +1 more source

Targeting MCL‐1 and MAPK overcomes venetoclax resistance in FLT3‐ITD‐positive AML cells harbouring activating PTPN11 (SHP‐2) mutations

open access: yesBritish Journal of Haematology, EarlyView.
Summary Venetoclax (VEN)‐based therapies have improved the treatment of acute myeloid leukaemia (AML); however, the emergence of resistance remains a major limitation. Mutations in protein tyrosine phosphatase (PTP) non‐receptor type 11 (PTPN11) and FMS like tyrosine kinase 3 with internal tandem duplication (FLT3‐ITD) are common in resistant patients ...
Maximilian Fleischmann   +12 more
wiley   +1 more source

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