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Adipocyte exosomes induce transforming growth factor beta pathway dysregulation in hepatocytes: a novel paradigm for obesity-related liver disease.
TLDR
Exosomes from VAT integrate into liver cells and induce dysregulation of TGF-β pathway members in vitro and offers an intriguing possibility for the pathogenesis of NAFLD.
Mechanisms of transforming growth factor β induced cell cycle arrest in palate development
TLDR
TGFβ1 and TGFβ3 play separate yet complimentary roles in achieving cell cycle arrest and EMT/apoptosis and cell cycle Arrest is a prerequisite for later cellular changes.
Dysregulation of upstream and downstream transforming growth factor-β transcripts in livers of children with biliary atresia and fibrogenic gene signatures.
TLDR
Gene transcripts for known upstream and downstream TGF-β mediators are differentially expressed in liver specimens from children with BA and a fibrogenic gene signature, and further investigation into whether these mediators may be attractive targets for future therapy inChildren with BA is warranted.
PAC1 regulates receptor tyrosine kinase transactivation in a reactive oxygen species-dependent manner
TLDR
The results show that ROS are essential for PAC1 to regulate EGFR and HER2 transactivation as well as proliferation of NSCLC cells.
Integrin &bgr;-8, But Not &bgr;-5 or -6, Protein Expression Is Increased in Livers of Children With Biliary Atresia
TLDR
Analysis of liver fibrosis and protein expression of the integrins in a larger cohort of patients with BA and compared them with patients undergoing liver biopsy for other diagnoses support the mounting evidence that transforming growth factor-&bgr; (TGF-& bgr;) activation is responsible for the fibrosis found in BA.
Targeting Extracellular Cyclophilins Ameliorates Disease Progression in Experimental Biliary Atresia
TLDR
The data provide the first evidence that extracellular cyclophilins activate the SMAD pathway and promote inflammation in experimental BA, and suggest that MM284 may be a promising therapeutic agent for treating BA and possibly other intrahepatic chronic disorders.
Molecular basis for high affinity and selectivity of peptide antagonist, Bantag-1, for the orphan BB3 receptor.
TLDR
This study systematically investigated the molecular basis for changes demonstrated in EC1, particularly important is the presence of aromatic-interactions by His(107), rather than hydrogen-bonding or charge-charge interactions, for determining Bantag-1 high affinity/selectivity.
[A model of the depressive syndrome in rats induced by the neurotoxin MPTP and autoantibodies to serotonin and dopamine].
TLDR
It is suggested that disturbances in neuroimmune interactions play an important part in development of depressive states.
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