Publications by authors named "Lagirand-Cantaloube Julie"
Article Synopsis
- In human eggs, the risk of aneuploidy (abnormal chromosome numbers) increases with age, leading to infertility and potential genetic disorders.
- Research indicates that in human eggs, as women age, the distances between kinetochores of chromosomes grow larger, causing issues during cell division (specifically in metaphase I and II).
- The spindle assembly checkpoint (SAC), which helps prevent chromosome mismanagement, appears to be less effective in older oocytes due to decreased localization of key proteins like BUB1 and BUBR1, contributing to aneuploidy.
The eukaryotic initiation factor 3 subunit f (eIF3f) is one of the 13 subunits of the translation initiation factor complex eIF3 required for several steps in the initiation of mRNA translation. In skeletal muscle, recent studies have demonstrated that eIF3f plays a central role in skeletal muscle size maintenance. Accordingly, eIF3f overexpression results in hypertrophy through modulation of protein synthesis via the mTORC1 pathway.
View Article and Find Full Text PDFIn skeletal muscle atrophy, upregulation and nuclear accumulation of the Ubiquitin E3 ligase MAFbx is essential for accelerated muscle protein loss, but the nuclear/cytoplasmic shuttling of MAFbx is undefined. Here we found that MAFbx contains two functional nuclear localization signals (NLS). Mutation or deletion of only one NLS induced cytoplasmic localization of MAFbx.
View Article and Find Full Text PDFEWS-FLI1 inhibits TNFalpha-induced NFkappaB-dependent transcription in Ewing sarcoma cells.
Biochem Biophys Res Commun
September 2010
Ewing sarcoma is primarily caused by a t(11;22) chromosomal translocation encoding the EWS-FLI1 fusion protein. To exert its oncogenic function, EWS-FLI1 acts as an aberrant transcription factor, broadly altering the gene expression profile of tumor cells. Nuclear factor-kappaB (NFkappaB) is a tightly regulated transcription factor controlling cell survival, proliferation and differentiation, as well as tumorigenesis.
View Article and Find Full Text PDFUbiquitin ligase Atrogin1/Muscle Atrophy F-box (MAFbx) up-regulation is required for skeletal muscle atrophy but substrates and function during the atrophic process are poorly known. The transcription factor MyoD controls myogenic stem cell function and differentiation, and seems necessary to maintain the differentiated phenotype of adult fast skeletal muscle fibres. We previously showed that MAFbx mediates MyoD proteolysis in vitro.
View Article and Find Full Text PDFArticle Synopsis
- The E3 ubiquitin ligase Atrogin1/MAFbx is significantly increased in response to systemic diseases like cancer and AIDS, contributing to muscle atrophy.
- During muscle wasting, MAFbx targets the eukaryotic initiation factor eIF3-f for degradation, which directly influences muscle size.
- Enhancing eIF3-f can promote muscle growth, while reducing it causes atrophy, suggesting that eIF3-f is a crucial player in regulating muscle mass and a potential target for therapies.