Overexpression of Eph transcripts has been observed in some carcinomas of the colon, lung, and liver. Eph is the largest family of receptor tyrosine kinases and most of the family members are expressed primarily, but not exclusively, in the nervous system. A cDNA was isolated that encodes Xek (Xenopus Elk-like Kinase), a tyrosine kinase receptor that appears to be ubiquitously expressed in adult tissues with higher expression observed in brain and ovary. In situ hybridization analysis demonstrates localized mRNA expression in the brain, branchial arches, trigeminal facial ganglion, and the post-mitotic retina cells of the swimming tadpole stage of development. Xek is an amphibian member of the Eph family, and may play a role in the development or function of the central nervous system. Recent studies have begun to identify ligands that can bind or activate members of the Eph family of receptor tyrosine kinases. These ligands described thus far are all membrane bound. Functional roles for the receptor-ligand interactions are beginning to be determined and suggest that they participate in axon bundling and guidance. We have isolated a cDNA encoding a putative ligand, termed Xlerk (Xenopus Ligand for Eph Receptor Kinases), that shows close homology with rat Lerk2 and has a very highly conserved intracellular domain. While there was some overlap in the expression pattern of the Xek receptor when compared to Xlerk, there also appears to be significant differences. Xlerk transcripts were observed in the olfactory placode, olfactory bulb, developing somites and innervations of the heart and gut (myenteric plexus). We have found that ectopic expression of Xlerk in the developing embryo causes the blastomeres of the embryo to disaggregate, suggesting a possible role in cell adhesion.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Intramural Research (Z01)
Project #
1Z01BC010006-01
Application #
2463807
Study Section
Special Emphasis Panel (LLB)
Project Start
Project End
Budget Start
Budget End
Support Year
1
Fiscal Year
1996
Total Cost
Indirect Cost
Name
National Cancer Institute Division of Basic Sciences
Department
Type
DUNS #
City
State
Country
United States
Zip Code
Lee, Hyun-Shik; Nishanian, Tagvor G; Mood, Kathleen et al. (2008) EphrinB1 controls cell-cell junctions through the Par polarity complex. Nat Cell Biol 10:979-86
Bong, Yong-Sik; Lee, Hyun-Shik; Carim-Todd, Laura et al. (2007) ephrinB1 signals from the cell surface to the nucleus by recruitment of STAT3. Proc Natl Acad Sci U S A 104:17305-10
Lee, Hyun-Shik; Bong, Yong-Sik; Moore, Kathryn B et al. (2006) Dishevelled mediates ephrinB1 signalling in the eye field through the planar cell polarity pathway. Nat Cell Biol 8:55-63
Ishimura, A; Lee, H-S; Bong, Y-S et al. (2006) Oncogenic Met receptor induces ectopic structures in Xenopus embryos. Oncogene 25:4286-99
Mood, Kathleen; Saucier, Caroline; Bong, Yong-Sik et al. (2006) Gab1 is required for cell cycle transition, cell proliferation, and transformation induced by an oncogenic met receptor. Mol Biol Cell 17:3717-28
Mood, Kathleen; Saucier, Caroline; Ishimura, Akihiko et al. (2006) Oncogenic Met receptor induces cell-cycle progression in Xenopus oocytes independent of direct Grb2 and Shc binding or Mos synthesis, but requires phosphatidylinositol 3-kinase and Raf signaling. J Cell Physiol 207:271-85
Mood, Kathleen; Bong, Yong-Sik; Lee, Hyun-Shik et al. (2004) Contribution of JNK, Mek, Mos and PI-3K signaling to GVBD in Xenopus oocytes. Cell Signal 16:631-42
Park, Eui Kyun; Warner, Neil; Bong, Yong-Sik et al. (2004) Ectopic EphA4 receptor induces posterior protrusions via FGF signaling in Xenopus embryos. Mol Biol Cell 15:1647-55
Bong, Yong-Sik; Park, Yeon-Hwa; Lee, Hyun-Shik et al. (2004) Tyr-298 in ephrinB1 is critical for an interaction with the Grb4 adaptor protein. Biochem J 377:499-507
Moore, Kathryn B; Mood, Kathleen; Daar, Ira O et al. (2004) Morphogenetic movements underlying eye field formation require interactions between the FGF and ephrinB1 signaling pathways. Dev Cell 6:55-67

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