scholarly journals The role of the Janus kinase family/signal transducer and activator of transcription signaling pathway in fibrotic renal disease

2012 ◽  
Vol 178 (1) ◽  
pp. 339-345 ◽  
Author(s):  
Futoshi Matsui ◽  
Kirstan K. Meldrum
Keyword(s):  
Renal Disease ◽  
Signaling Pathway ◽  
Janus Kinase ◽  
Signal Transducer ◽  
Kinase Family

scholarly journals The JAK/STAT signaling pathway: from bench to clinic

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Xiaoyi Hu ◽  
Jing li ◽  
Maorong Fu ◽  
Xia Zhao ◽  
Wei Wang
Keyword(s):  
Signaling Pathway ◽  
Current Knowledge ◽  
Janus Kinase ◽  
Signal Transducer ◽  
Quarter Century ◽  
Cellular Processes ◽  
Stat Signaling ◽  
Cancer And Inflammation ◽  
Stat Pathway

AbstractThe Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway was discovered more than a quarter-century ago. As a fulcrum of many vital cellular processes, the JAK/STAT pathway constitutes a rapid membrane-to-nucleus signaling module and induces the expression of various critical mediators of cancer and inflammation. Growing evidence suggests that dysregulation of the JAK/STAT pathway is associated with various cancers and autoimmune diseases. In this review, we discuss the current knowledge about the composition, activation, and regulation of the JAK/STAT pathway. Moreover, we highlight the role of the JAK/STAT pathway and its inhibitors in various diseases.

Atomistic insight into the inhibition mechanisms of suppressors of cytokine signaling on Janus kinase

2019 ◽  
Vol 21 (24) ◽  
pp. 12905-12915 ◽  
Author(s):  
Yaru Wei ◽  
Zhiyang Zhang ◽  
Nai She ◽  
Xin Chen ◽  
Yuan Zhao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Negative Feedback ◽  
Janus Kinase ◽  
Cytokine Signaling ◽  
Signal Transducer ◽  
Jak Kinase ◽  
Stat Signaling ◽  
Suppressors Of Cytokine Signaling ◽  
Insight Into

Suppressors of cytokine signaling (SOCS) act as negative feedback regulators of the Janus kinase/signal transducer (JAK–STAT) signaling pathway by inhibiting the activity of JAK kinase.

scholarly journals JAK/STAT Activation: A General Mechanism for Bone Development, Homeostasis, and Regeneration

2020 ◽  
Vol 21 (23) ◽  
pp. 9004
Author(s):  
Alexandra Damerau ◽  
Timo Gaber ◽  
Sarah Ohrndorf ◽  
Paula Hoff
Keyword(s):  
Signaling Pathway ◽  
Bone Development ◽  
Gene Knockout ◽  
Selective Inhibition ◽  
Janus Kinase ◽  
General Mechanism ◽  
Stat Signaling ◽  
Skeletal Phenotype ◽  
Pro Inflammatory Cytokines

The Janus kinase (JAK) signal transducer and activator of transcription (STAT) signaling pathway serves as an important downstream mediator for a variety of cytokines, hormones, and growth factors. Emerging evidence suggests JAK/STAT signaling pathway plays an important role in bone development, metabolism, and healing. In this light, pro-inflammatory cytokines are now clearly implicated in these processes as they can perturb normal bone remodeling through their action on osteoclasts and osteoblasts at both intra- and extra-articular skeletal sites. Here, we summarize the role of JAK/STAT pathway on development, homeostasis, and regeneration based on skeletal phenotype of individual JAK and STAT gene knockout models and selective inhibition of components of the JAK/STAT signaling including influences of JAK inhibition in osteoclasts, osteoblasts, and osteocytes.

Endoplasmic Reticulum Stress Prolongs GH-Induced Janus Kinase (JAK2)/Signal Transducer and Activator of Transcription (STAT5) Signaling Pathway

2001 ◽  
Vol 15 (9) ◽  
pp. 1471-1483 ◽  
Author(s):  
Amilcar Flores-Morales ◽  
Leandro Fernández ◽  
Elizabeth Rico-Bautista ◽  
Adriana Umana ◽  
Ciro Negrín ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Signaling Pathway ◽  
Janus Kinase ◽  
Signal Transducer

scholarly journals The role of signal transducer and activator of transcription 5 in the inhibitory effects of GH on adipocyte differentiation

2003 ◽  
Vol 30 (2) ◽  
pp. 139-150 ◽  
Author(s):  
HE Richter ◽  
T Albrektsen ◽  
N Billestrup
Keyword(s):  
Tyrosine Phosphorylation ◽  
Janus Kinase ◽  
Peroxisome Proliferator ◽  
Transactivation Domain ◽  
Signal Transducer ◽  
Inhibitory Effects ◽  
Preadipocyte Differentiation ◽  
Peroxisome Proliferator Activated Receptor ◽  
Fatty Acid Binding

GH inhibits primary rat preadipocyte differentiation and expression of late genes required for terminal differentiation. Here we show that GH-mediated inhibition of fatty acid-binding protein aP2 gene expression correlates with the activation of the Janus kinase-2/signal transducer and activator of transcription (STAT)-5 signalling pathway. Within minutes of treatment, GH induced the tyrosine phosphorylation, nuclear localization and DNA binding of STAT5. Importantly, there was no evidence that STAT5 acted via an interaction with peroxisome proliferator-activated receptor gamma. To further understand the mechanism of STAT5 action, we reconstituted the inhibition of aP2 in a non-adipogenic cell line. Using this system, we showed that the ability of GH to inhibit a 520 bp aP2 reporter was largely dependent upon the presence of either STAT5A or STAT5B. Mutant analysis confirmed that the tyrosine phosphorylation of STAT5 was essential for this signalling. However, STAT5's C-terminal transactivation domain was fully dispensable for this inhibition. Taken together, these data confirm a key regulatory role of STAT5 in adipose tIssue and point to STAT5 as the repressing modulator of GH-mediated inhibition in primary preadipocytes.

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