Embryonic stem cells express multiple Eph-subfamily receptor tyrosine kinases
- Author(s)
- Lickliter, JD; Smith, FM; Olsson, JE; Mackwell, KL; Boyd, AW;
- Details
- Publication Year 1996-01-09,Volume 93,Issue #1,Page 145-150
- Journal Title
- PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Publication Type
- Journal Article
- Abstract
- Eph and its homologues form the largest subfamily of receptor tyrosine kinases. Normal expression patterns of this subfamily indicate roles in differentiation and development, whereas their overexpression has been linked to oncogenesis, This study investigated the potential role of Eph-related molecules during very early embryonic development by examining their expression in embryonic stem (ES) cells and embryoid bodies differentiated from ES cells in vitro. By use of a strategy based on reverse transcriptase-mediated PCR, nine clones containing Eph-subfamily sequence were isolated from ES cells, Of these, eight were almost identical to one of four previously identified molecules (Sek, Nuk, Eck, and Mek4). However, one clone contained sequence from a novel Eph-subfamily member, which was termed embryonic stem-cell kinase or Esk., Northern analysis showed expression of Esk in ES cells, embryoid bodies, day 12 mouse embryos, and some tissues of the adult animal. Levels of expression were similar in ES cells and embryoid bodies, By comparison, Mek4 showed no significant transcription in the ES cell cultures by Northern analysis, whereas Eck displayed stronger signals in ES cells than in the embryoid bodies. These results suggest that Eph-subfamily molecules may play roles during the earliest phases of embryogenesis. Furthermore, the relative importance of different members of this subfamily appears to change as development proceeds.
- Publisher
- NATL ACAD SCIENCES
- Keywords
- GENE; FAMILY; IDENTIFICATION; CHICKEN; CLONING; MEMBERS; MOUSE; HEK
- Publisher's Version
- https://doi.org/10.1073/pnas.93.1.145
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1996-01-09 12:00:00