Phosphate-activated cyclin-dependent kinase stabilizes G1 cyclin to trigger cell cycle entry

G1 cyclins, in association with a cyclin-dependent kinase (CDK), are universal activators of the transcriptional G1-S machinery during entry into the cell cycle. Regulation of cyclin degradation is crucial for coordinating progression through the cell cycle, but the mechanisms that modulate cyclin stability to control cell cycle entry are still unknown. Here, we show that a lack of phosphate downregulates Cln3 cyclin and leads to G1 arrest in Saccharomyces cerevisiae. The stability of Cln3 protein is diminished in strains with low activity of Pho85, a phosphate-sensing CDK. Cln3 is an in vitro substrate of Pho85, and both proteins interact in vivo. More interestingly, cells that carry a CLN3 allele encoding aspartic acid substitutions at the sites of Pho85 phosphorylation maintain high levels of Cln3 independently of Pho85 activity. Moreover, these cells do not properly arrest in G1 in the absence of phosphate and they die prematurely. Finally, the activity of Pho85 is essential for accumulating Cln3 and for reentering the cell cycle after phosphate refeeding. Taken together, our data indicate that Cln3 is a molecular target of the Pho85 kinase that is required to modulate cell cycle entry in response to environmental changes in nutrient availability. © 2013, American Society for Microbiology.S. Hernández received a postgraduate Junior Faculty fellowship from the UIC and l'Obra Social la Caixa. This work was supported by grants from Ministerio de Ciencia e Innovación of the Spanish government (BFU 2009-09278)Peer Reviewe

Totally laparoscopic aortic repair: A new device for direct transperitoneal approach

On the basis of our experience with more than 71 cases of totally laparoscopic aortic surgery by the retrocolic approach, we have developed a new technique by a simple transperitoneal approach. The purpose of this report is to describe that technique and the novel laparoscopic bowel retractor used to ensure stable exposure of the aorta

Traction Forces of Endothelial Cells under Slow Shear Flow

Endothelial cells are constantly exposed to fluid shear stresses that regulate vascular morphogenesis, homeostasis, and disease. The mechanical responses of endothelial cells to relatively high shear flow such as that characteristic of arterial circulation has been extensively studied. Much less is known about the responses of endothelial cells to slow shear flow such as that characteristic of venous circulation, early angiogenesis, atherosclerosis, intracranial aneurysm, or interstitial flow. Here we used a novel, to our knowledge, microfluidic technique to measure traction forces exerted by confluent vascular endothelial cell monolayers under slow shear flow. We found that cells respond to flow with rapid and pronounced increases in traction forces and cell-cell stresses. These responses are reversible in time and do not involve reorientation of the cell body. Traction maps reveal that local cell responses to slow shear flow are highly heterogeneous in magnitude and sign. Our findings unveil a low-flow regime in which endothelial cell mechanics is acutely responsive to shear stress

Corrigendum to 'Editor's Choice - European Society for Vascular Surgery (ESVS) 2020 Clinical Practice Guidelines on the Management of Vascular Graft and Endograft Infections' [European Journal of Vascular & Endovascular Surgery 59/3 (2020) 339-384]

peer reviewe

Editor's Choice - European Society for Vascular Surgery (ESVS) 2020 Clinical Practice Guidelines on the Management of Vascular Graft and Endograft Infections.

peer reviewe

How to manage hypertension with atherosclerotic renal artery stenosis?

The management of atherosclerotic renal artery stenosis (ARAS) in patients with hypertension has been the topic of great controversy. Major contemporary clinical trials such as the Cardiovascular Outcomes for Renal Artery lesions (CORAL) and Angioplasty and Stenting for Renal Atherosclerotic lesions (ASTRAL) have failed to show significant benefit of revascularization over medical management in controlling blood pressure and preserving renal function. We present here the implications and limitations of these trials and formulate recommendations for management of ARAS

sj-tiff-4-jet-10.1177_15266028231169172 – Supplemental material for Outcomes of Secondary Endovascular Aortic Repair After Frozen Elephant Trunk

Supplemental material, sj-tiff-4-jet-10.1177_15266028231169172 for Outcomes of Secondary Endovascular Aortic Repair After Frozen Elephant Trunk by Aurélien Hostalrich, Jean Porterie, Thibaut Boisroux, Bertrand Marcheix, Jean Baptiste Ricco and Xavier Chaufour in Journal of Endovascular Therapy</p

sj-tif-2-jet-10.1177_15266028231169172 – Supplemental material for Outcomes of Secondary Endovascular Aortic Repair After Frozen Elephant Trunk

Supplemental material, sj-tif-2-jet-10.1177_15266028231169172 for Outcomes of Secondary Endovascular Aortic Repair After Frozen Elephant Trunk by Aurélien Hostalrich, Jean Porterie, Thibaut Boisroux, Bertrand Marcheix, Jean Baptiste Ricco and Xavier Chaufour in Journal of Endovascular Therapy</p