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Geneviève Kayser Paul Lambotte Paul Falmagne Carine Capiau Jacqueline Zanen Jean-Marie Ruysschaert 《Biochemical and biophysical research communications》1981,99(2):358-363
Conductance measurements on planar lipid bilayers demonstrate that CB1, a CNBr peptide of diphtheria toxin fragment B located in its middle region, possesses the unique property to destabilize the lipid bilayer organization. It is suggested that a segment of 25 amino acids in the N-terminal sequence of CB1 could be responsible for this effect. Its very low polarity, its predicted amphipathic helical structure and a helix length corresponding to the thickness of the hydrocarbon region of the lipid bilayer should specifically favor its insertion in the membrane. The existence of such a transverse lipid-associating domain could confer upon the molecule the properties leading to the anchoring of diphtheria toxin in the cytoplasmic membrane. 相似文献
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Baron Cécile Nguyen Vu-Hieu Naili Salah Guivier-Curien Carine 《Biomechanics and modeling in mechanobiology》2020,19(5):1755-1764
Biomechanics and Modeling in Mechanobiology - Ultrasound stimulation is thought to influence bone remodelling process. But recently, the efficiency of ultrasound therapy for bone healing has been... 相似文献
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Frappier Martin Auclair Julie Bouasker Samir Gunaratnam Sathursha Diarra Carine Millette Mathieu 《Probiotics and antimicrobial proteins》2022,14(5):873-883
Probiotics and Antimicrobial Proteins - Dyslipidemia, specifically abnormal levels of low-density lipoprotein cholesterol (LDL-C), is an important risk factor of cardiovascular disease. Evidence... 相似文献
207.
Gilles Darcis Anna Kula Sophie Bouchat Koh Fujinaga Francis Corazza Amina Ait-Ammar Nadège Delacourt Adeline Melard Kabamba Kabeya Caroline Vanhulle Benoit Van Driessche Jean-Stéphane Gatot Thomas Cherrier Luiz F. Pianowski Lucio Gama Christian Schwartz Jorge Vila Arsène Burny Nathan Clumeck Michel Moutschen Stéphane De Wit B. Matija Peterlin Christine Rouzioux Olivier Rohr Carine Van Lint 《PLoS pathogens》2015,11(7)
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Padma Murthi Sophie Brouillet Anita Pratt Anthony Borg Bill Kalionis Frederic Goffin Vassilis Tsatsaris Carine Munaut Jean-Jacques Feige Mohamed Benharouga Thierry Fournier Nadia Alfaidy 《Molecular medicine (Cambridge, Mass.)》2015,21(1):645-656
Idiopathic fetal growth restriction (FGR) is frequently associated with placental insufficiency. Previous reports have provided evidence that endocrine gland–derived vascular endothelial growth factor (EG-VEGF), a placental secreted protein, is expressed during the first trimester of pregnancy, controls both trophoblast proliferation and invasion, and its increased expression is associated with human FGR. In this study, we hypothesize that EG-VEGF-dependent changes in placental homeobox gene expressions contribute to trophoblast dysfunction in idiopathic FGR. The changes in EG-VEGF-dependent homeobox gene expressions were determined using a homeobox gene cDNA array on placental explants of 8–12 wks gestation after stimulation with EG-VEGF in vitro for 24 h. The homeobox gene array identified a greater-than-five-fold increase in HOXA9, HOXC8, HOXC10, HOXD1, HOXD8, HOXD9 and HOXD11, while NKX 3.1 showed a greater-than-two-fold decrease in mRNA expression compared with untreated controls. Homeobox gene NKX3.1 was selected as a candidate because it is a downstream target of EG-VEGF and its expression and functional roles are largely unknown in control and idiopathic FGR-affected placentae. Real-time PCR and immunoblotting showed a significant decrease in NKX3.1 mRNA and protein levels, respectively, in placentae from FGR compared with control pregnancies. Gene inactivation in vitro using short-interference RNA specific for NKX3.1 demonstrated an increase in BeWo cell differentiation and a decrease in HTR-8/SVneo proliferation. We conclude that the decreased expression of homeobox gene NKX3.1 downstream of EG-VEGF may contribute to the trophoblast dysfunction associated with idiopathic FGR pregnancies. 相似文献
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ManTek Yeung Rose Hurren Carine Nemr Xiaoming Wang Samantha Hershenfeld Marcela Gronda Sanduni Liyanage Yan Wu Jeevan Augustine Eric A. Lee Paul A. Spagnuolo Noel Southall Catherine Chen Wei Zheng Danny V. Jeyaraju Mark D. Minden Rebecca Laposa Aaron D. Schimmer 《Apoptosis : an international journal on programmed cell death》2015,20(6):811-820
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van Staveren WC Beeckman S Tomás G Dom G Hébrant A Delys L Vliem MJ Trésallet C Andry G Franc B Libert F Dumont JE Maenhaut C 《Experimental cell research》2012,318(5):444-452
cAMP pathway activation by thyrotropin (TSH) induces differentiation and gene expression in thyrocytes. We investigated which partners of the cAMP cascade regulate gene expression modulations: protein kinase A and/or the exchange proteins directly activated by cAMP (Epac). Human primary cultured thyrocytes were analysed by microarrays after treatment with the adenylate cyclase activator forskolin, the protein kinase A (PKA) activator 6-MB-cAMP and the Epac-selective cAMP analog 8-pCPT-2'-O-Me-cAMP (007) alone or combined with 6-MB-cAMP. Profiles were compared to those of TSH. Cultures treated with the adenylate cyclase- or the PKA activator alone or the latter combined with 007 had profiles similar to those induced by TSH. mRNA profiles of 007-treated cultures were highly distinct from TSH-treated cells, suggesting that TSH-modulated gene expressions are mainly modulated by cAMP and PKA and not through Epac in cultured human thyroid cells. To investigate whether the Epac-Rap-RapGAP pathway could play a potential role in thyroid tumorigenesis, the mRNA expressions of its constituent proteins were investigated in two malignant thyroid tumor types. Modulations of this pathway suggest an increased Rap pathway activity in these cancers independent from cAMP activation. 相似文献