Results 51 to 60 of about 73,607 (303)

Emerging systemic JAK inhibitors in the treatment of atopic dermatitis: a review of abrocitinib, baricitinib, and upadacitinib

open access: yesDrugs in Context, 2020
The Janus kinases (JAK) are a group of molecules, composed of JAK1, JAK2, JAK3, and tyrosine kinase 2 (TYK2), which are key components within the JAK–signal transducers and activators of transcription pathway, where cytokine receptor signaling takes ...
Novin Nezamololama   +3 more
doaj   +1 more source

Management of MPN beyond JAK2 [PDF]

open access: yesHematology, 2014
Abstract Thrombocytosis has a large number of potential underlying causes, but the dominant group of hematological conditions for consideration in this setting are the myeloproliferative neoplasms (MPNs). In this chapter, we consider several key linked questions relating to the management of thrombocytosis in MPNs and discuss several ...
Claire N, Harrison   +1 more
openaire   +2 more sources

Heat-shock protein 70 and pentraxin-3 inflammatory biomarkers: Implication for thrombosis in polycythemia vera

open access: yesIraqi Journal of Hematology, 2020
BACKGROUND: Chronic inflammation has been suggested to contribute to the pathogenesis of thrombosis in polycythemia vera (PV) as it triggers in vivo activation of platelets, leukocytes, and endothelial cells, which are all of major importance during ...
Ibrahim Abdullah Mahmood   +2 more
doaj   +1 more source

The human myeloproliferative disorders: molecular pathogenesis and clonal heterogeneity

open access: yes, 2010
The classical myeloproliferative disorders (MPD), comprising essential thrombocythaemia (ET), polycythaemia vera (PV) and idiopathic myelofibrosis (IMF), are clonal premalignant haematopoietic neoplasms associated with activating mutations in signalling ...

core   +1 more source

Dual targeting of JAK2 and ERK interferes with the myeloproliferative neoplasm clone and enhances therapeutic efficacy. [PDF]

open access: yes, 2021
Myeloproliferative neoplasms (MPN) show dysregulated JAK2 signaling. JAK2 inhibitors provide clinical benefits, but compensatory activation of MAPK pathway signaling impedes efficacy.
Levine, Ross L   +14 more
core   +1 more source

The SH2 domain and kinase activity of JAK2 target JAK2 to centrosome and regulate cell growth and centrosome amplification.

open access: yesPLoS ONE, 2022
JAK2 is cytokine-activated non-receptor tyrosine kinase. Although JAK2 is mainly localized at the plasma membrane, it is also present on the centrosome. In this study, we demonstrated that JAK2 localization to the centrosome depends on the SH2 domain and
Aashirwad Shahi   +3 more
doaj   +1 more source

Downregulation of ClC-2 by JAK2 [PDF]

open access: yesCellular Physiology and Biochemistry, 2012
JAK2 (Janus kinase-2) is activated by cell shrinkage and may thus participate in cell volume regulation. Cell volume regulatory ion channels include the small conductance Cl(-) channels ClC-2. The present study thus explored whether JAK2 influences ClC-2 activity.
Hosseinzadeh, Zohreh   +2 more
openaire   +3 more sources

Enu mutagenesis identifies a novel platelet phenotype in a loss-of-function Jak2 allele. [PDF]

open access: yesPLoS ONE, 2013
Utilizing ENU mutagenesis, we identified a mutant mouse with elevated platelets. Genetic mapping localized the mutation to an interval on chromosome 19 that encodes the Jak2 tyrosine kinase.
Nicole M Anderson   +16 more
doaj   +1 more source

Rewriting the mechanism of JAK2 activation [PDF]

open access: yesCell Cycle, 2015
Class I cytokine receptors regulate a wide range of clinically relevant cellular processes. This family of receptors contains around 30 members including receptors for erythropoietin (EPO), prolactin (PRL), growth hormone (GH), thrombopoietin (TPO), granulocyte-macrophage colony-stimulating factor (GM-CSF), leukemia inhibitory factor (LIF), interleukin-
Brooks, Andrew J., Waters, Michael J.
openaire   +5 more sources

Aging Is a Key Driver for Adult Acute Myeloid Leukemia

open access: yesAging and Cancer, EarlyView.
Acute myeloid leukemia (AML) is a classical age‐related hematologic malignancy, and a key driver of AML is aging, which profoundly regulates intrinsic factors such as genomic instability, epigenetic reprogramming, and metabolic dysregulation, and alters bone marrow microenvironment.
Rong Yin, Haojian Zhang
wiley   +1 more source

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