Female-Specific Role of Ciliary Neurotrophic Factor in the Medial Amygdala in Regulating Stress Responses

2021 ◽  
Author(s):  
cuihong jia ◽  
W. Drew Gill ◽  
Chiharu Lovins ◽  
Theo Hagg ◽  
Russell R. Brown

2012 ◽  
Vol 159B (7) ◽  
pp. 786-793 ◽  
Author(s):  
Andreas Reif ◽  
Heike Weber ◽  
Katharina Domschke ◽  
Benedikt Klauke ◽  
Christian Baumann ◽  
...  


1998 ◽  
Vol 90 (1) ◽  
pp. 49
Author(s):  
S.W. Levison ◽  
P.J. Albrecht ◽  
S.N. Hudgins ◽  
M.H. Ducceschi ◽  
T.L. Wood


2010 ◽  
Vol 86 (3) ◽  
pp. 261-270 ◽  
Author(s):  
Narelle E. McGregor ◽  
Ingrid J. Poulton ◽  
Emma C. Walker ◽  
Sueli Pompolo ◽  
Julian M. W. Quinn ◽  
...  


2020 ◽  
Vol 64 (4) ◽  
Author(s):  
Sonia Fantone ◽  
Giovanni Tossetta ◽  
Rodolfo Montironi ◽  
Martina Senzacqua ◽  
Daniela Marzioni ◽  
...  

Ciliary neurotrophic factor (CNTF) is a member of interleukin-6 type cytokine family. The CNTF receptor complex is a heterodimer including gp130 and CNTF receptor α (CNTFRα) proteins triggering the activation of multiple intracellular signaling pathways including AKT/PI3K, MAPK/ERK and Jak/STAT pathways. At present no data are available on the localization of CNTF and CNTFRα in prostate as well as on the role of CNTF in this organ. In this study we have analyzed the localization of CNTF and CNTFRα by immunohistochemistry and we have used PWR-1E cell line as a model for normal glandular cell to investigate the role of this cytokine. Our results show that CNTF and CNTFRa are expressed in the staminal compart of the prostate and that CNTF selectively inhibits ERK pathway. In conclusion, we suggest that CNTF could be considered as key molecule to maintenance epithelium homeostasis via pERK downregulation by an autocrine mechanism. Further CNTF studies in prostate cancer could be useful to verify the potential role of this cytokine in carcinogenesis.



2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Anne Ruiz ◽  
Sevasti Gaspari ◽  
Lorna Farrelly ◽  
Claire Polizu ◽  
kerri pryce ◽  
...  


2013 ◽  
Vol 37 (3) ◽  
pp. 587-592 ◽  
Author(s):  
Jun Ding ◽  
Zhili He ◽  
Juan Ruan ◽  
Zilong Ma ◽  
Ying Liu ◽  
...  


2013 ◽  
Vol 92 (5) ◽  
pp. 493-493
Author(s):  
Narelle E. McGregor ◽  
Ingrid J. Poulton ◽  
Emma C. Walker ◽  
Sueli Pompolo ◽  
Julian M. W. Quinn ◽  
...  




2016 ◽  
Vol 36 (8) ◽  
pp. 1272-1286 ◽  
Author(s):  
Jakob Vejby Larsen ◽  
Anders Mejer Kristensen ◽  
Lone Tjener Pallesen ◽  
Johannes Bauer ◽  
Christian Bjerggaard Vægter ◽  
...  

Cardiotrophin-like cytokine:cytokine-like factor-1 (CLC:CLF-1) is a heterodimeric neurotropic cytokine that plays a crucial role during neuronal development. Mice lacking CLC:CLF-1 die soon after birth due to a suckling defect and show reduced numbers of motor neurons. Humans carrying mutations in CLC:CLF-1 develop similar disorders, known as Sohar-Crisponi or cold-induced sweating syndrome, and have a high risk of early death. It is well known that CLC binds the ciliary neurotrophic factor receptor α (CNTFRα) and is a prerequisite for signaling through the gp130/leukemia inhibitory factor receptor β (LIFRβ) heterodimer, whereas CLF-1 serves to promote the cellular release of CLC. However, the precise role of CLF-1 is unclear. Here, we report that CLF-1, based on its binding site for CLC and on two additional and independent sites for CNTFRα and sorLA, is a key player in CLC and CNTFRα signaling and turnover. The site for CNTFRα enables CLF-1 to promote CLC:CNTFRα complex formation and signaling. The second site establishes a link between the endocytic receptor sorLA and the tripartite CLC:CLF-1:CNTFRα complex and allows sorLA to downregulate the CNTFRα pool in stimulated cells. Finally, sorLA may bind and concentrate the tripartite soluble CLC:CLF-1:CNTFRα complex on cell membranes and thus facilitate its signaling through gp130/LIFRβ.



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