News
Select Category
| All Entries | New Antibodies | Research News | About antibodies-online.com |
Autophagy Is Essential for Preimplantation Development of Mouse Embryos
Areas: Metabolism
Autophagic degradation within early embryos seems to be essential for preimplantation development in mammals. A research group from the Tokyo Medical and Dental University, Japan analysed the degradation of maternal proteins in oocytes upon fertilisation.
Usually, maternal proteins are degraded in oocytes after fertilisation and new proteins are synthesised that are encoded by the new zygotic genome. The scientists found that autophagy, a catabolic process to degrade cell's own components in its lysosomes, was triggered by fertilisation and up-regulated in early murine embryos.
Atg5 (autophagy-related 5) knockout mice were used to obtain autophagy-defective oocytes. Those oocytes were unable to develop further than four- or eight-cell stages if they were fertilised with Atg5 -/- sperm. Fertilisation with wild-type sperm resulted in normal development of the embryos. The rate of protein synthesis was reduced in Atg5 -/- embryos.
Related antibodies on antibodies-online.com:
Atg5 (Saccharomyces cerevisiae)
Antibodies for the research area metabolism: »Show antibodies
-

13.11.2008 Hepatocyte-specific ablation of Foxa2 alters bile acid homeostasis and results in endoplasmic reticulum stress -

13.11.2008 Effective induction of high-titer antibodies by viral vector vaccines -

03.11.2008 Y-box-1 protein (Yb-1) and breast cancer: Prognostic factor and target for therapy -

28.10.2008 NALP3 inflammasome is involved in the innate immune response to amyloid-beta -

28.10.2008 Adenovirus Small e1a Alters Global Patterns of Histone Modification -

28.10.2008 Plant Immunity Requires Conformational Charges of NPR1 via S-Nitrosylation and Thioredoxins -

28.10.2008 The Spread of Ras Activity Triggered by Activation of a Single Dendritic Spine -

09.10.2008 Modulation of Gene Expression via Disruption of NF-kappa-B Signaling by a Bacterial Small Molecule -

09.10.2008 Anomalous Type 17 Response to Viral Infection by CD8+ T Cells Lacking T-bet and Eomesodermin







