Results 11 to 20 of about 28,299 (224)

Grb7 Protein Stability Modulated by Pin1 in Association with Cell Cycle Progression. [PDF]

open access: yesPLoS ONE, 2016
Growth factor receptor bound protein-7 (Grb7) is a multi-domain adaptor protein that is co-opted by numerous tyrosine kinases involved in various cellular signaling and functions. The molecular mechanisms underlying the regulation of Grb7 remain unclear.
Yu-Ling Tai   +9 more
doaj   +1 more source

Inhibition of the Activity of Cyclophilin A Impedes Prolactin Receptor-Mediated Signaling, Mammary Tumorigenesis, and Metastases

open access: yesiScience, 2020
Summary: Prolactin (PRL) and its receptor (PRLr) play important roles in the pathogenesis of breast cancer. Cyclophilin A (CypA) is a cis-trans peptidyl-prolyl isomerase (PPI) that is constitutively associated with the PRLr and facilitates the activation
Shawn Hakim   +3 more
doaj   +1 more source

Ligand-specific conformational change drives interdomain allostery in Pin1

open access: yesNature Communications, 2022
Born et al. describe interdomain allostery in the two domain peptidyl-prolyl isomerase Pin1 upon binding of two ligands. These ligands couple population shifts of extended and compact states to changes in the catalytic site of Pin1.
Alexandra Born   +6 more
doaj   +1 more source

Prolyl isomerase Pin1 in cancer [PDF]

open access: yesCell Research, 2014
Proline-directed phosphorylation is a posttranslational modification that is instrumental in regulating signaling from the plasma membrane to the nucleus, and its dysregulation contributes to cancer development. Protein interacting with never in mitosis A1 (Pin1), which is overexpressed in many types of cancer, isomerizes specific phosphorylated Ser ...
Zhimin, Lu, Tony, Hunter
openaire   +2 more sources

Pin1 inhibition improves the efficacy of ralaniten compounds that bind to the N-terminal domain of androgen receptor

open access: yesCommunications Biology, 2021
Leung et al. find that the peptidyl-prolyl isomerase Pin1 targets the intrinsically disordered N-terminal domain of the androgen receptor (AR). They show that combining Pin1 inhibition with ralaniten compounds that bind to the AR N-terminal domain has ...
Jacky K. Leung   +5 more
doaj   +1 more source

Phosphate-Induced Renal Fibrosis Requires the Prolyl Isomerase Pin1. [PDF]

open access: yesPLoS ONE, 2016
Tubulo-interstitial fibrosis is a common, destructive endpoint for a variety of kidney diseases. Fibrosis is well correlated with the loss of kidney function in both humans and rodents.
Zhong-Jian Shen   +4 more
doaj   +1 more source

Structural and Functional Insights into Human Nuclear Cyclophilins

open access: yesBiomolecules, 2018
The peptidyl prolyl isomerases (PPI) of the cyclophilin type are distributed throughout human cells, including eight found solely in the nucleus. Nuclear cyclophilins are involved in complexes that regulate chromatin modification, transcription, and pre ...
Caroline Rajiv, Tara L. Davis
doaj   +1 more source

NmPin from the marine thaumarchaeote Nitrosopumilus maritimus is an active membrane associated prolyl isomerase. [PDF]

open access: yes, 2016
We cordially thank Alma Rute for excellent technical assistance and the DFG (GRK 1431-1 and 1431-2) for financial support (PB). We thank the Microscope and Histology Facility of the University of Aberdeen for providing their equipment.
Bayer, Peter   +5 more
core   +2 more sources

Editorial: Peptidyl-Prolyl Isomerases in Human Pathologies [PDF]

open access: yesFrontiers in Pharmacology, 2019
Editorial on the Research Topic: Peptidyl-prolyl Isomerases in Human ...
Tiziano Tuccinardi   +2 more
openaire   +3 more sources

Depletion of mitochondrial methionine adenosyltransferase α1 triggers mitochondrial dysfunction in alcohol-associated liver disease

open access: yesNature Communications, 2022
Lower activity of MATα1, which catalyzes the synthesis of the methyl donor S-adenosylmethionine, and mitochondrial dysfunction occur in alcohol-associated liver disease (ALD).
Lucía Barbier-Torres   +21 more
doaj   +1 more source

Home - About - Disclaimer - Privacy