derailed is required for muscle attachment site selection in Drosophila

Development ◽  
1996 ◽  
Vol 122 (9) ◽  
pp. 2761-2767 ◽  
Author(s):  
C.A. Callahan ◽  
J.L. Bonkovsky ◽  
A.L. Scully ◽  
J.B. Thomas

During development, muscles must form and attach at highly stereotyped positions to allow for coordinated movements. In Drosophila, muscles grow towards and attach to specifically positioned cells within the epidermis. At the molecular level, very little is known about how muscles recognize these attachment sites. The derailed gene encodes a receptor tyrosine kinase family member that is essential for the pathfinding ability of expressing neurons. Here we show that the Drl RTK is also expressed by a small subset of developing embryonic muscles and neighboring epidermal cells during muscle attachment site selection. In drl mutants, these muscles often fail to attach at appropriate locations although their epidermal attachment cells appear unaffected. These results show that, similar to its role in neuronal pathway recognition, the Drl RTK participates in a mechanism required for muscle attachment site selection. The data suggest that both neurons and muscles use common mechanisms to recognize their paths or targets, and that Drl plays an analogous role in both developing systems.


2013 ◽  
Vol 4 (5) ◽  
pp. 689 ◽  
Author(s):  
Nicole Teller ◽  
Matthias Roth ◽  
Melanie Esselen ◽  
Diana Fridrich ◽  
Ute Boettler ◽  
...  


1995 ◽  
Vol 73 (3-4) ◽  
pp. 133-136 ◽  
Author(s):  
Haleh Vahidi Samiei

Many laboratories, using a variety of organisms, have contributed to deciphering the identity and the order of the components leading from ligand-bound receptor tyrosine kinases to various intracellular events, including changes in gene expression. The gaps have only been filled recently. This minireview summarizes the findings and points out the degree of conservation of the same pathway in distant organisms, both at the molecular level and in terms of the consecutive steps. The review also looks at points at which this pathway might be diverging and points onto which other pathways might be converging. These interactions are not always clear cut, and understanding them will be the challenge for the future.Key words: signal transduction, receptor tyrosine kinase, RAS, RAF, MAP kinase.



Author(s):  
David J. Easty ◽  
Philip J. Mitchell ◽  
Ketan Patel ◽  
Vivi Ann Florenes ◽  
Richard A. Spritz ◽  
...  


2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Daniela I. Korec ◽  
Darian S. Louke ◽  
Justin T. Breitbach ◽  
Jennifer A. Geisler ◽  
Brian D. Husbands ◽  
...  

Abstract Background Urothelial carcinoma (UC) accounts for > 90% of canine tumors occurring in the urinary bladder. Toceranib phosphate (TOC) is a multi-target receptor tyrosine kinase (RTK) inhibitor that exhibits activity against members of the split kinase family of RTKs. The purpose of this study was to evaluate primary UC tumors and UC cell lines for the expression and activation of VEGFR2, PDGFRα, PDGFRβ, and KIT to assess whether dysregulation of these RTKs may contribute to the observed biological activity of TOC. Results Transcript for VEGFR2, PDGFRα, PDGFRβ, and KIT was detected in all UC tissue samples and UC cell lines. The Proteome Profiler™ Human Phospho-RTK Array Kit (R & D Systems) provided a platform to assess phosphorylation of 42 different RTKs in primary UC tumors and UC cell lines. Evidence of PDGFRα and PDGFRβ phosphorylation was present in only 11% or 33% of UC tumors, respectively, and 25% of UC cell lines. Treatment of UC cell lines with TOC had no significant impact on cell proliferation, including UC cell lines with evidence of PDGFRβ phosphorylation. Conclusions Phosphorylation of several key RTKs targeted by TOC is present in a small subset of primary UC tumors and UC cell lines, suggesting that these RTKs do not exist in a state of continuous activation. These data suggest that activation of RTKs targeted by TOC is present in a small subset of UC tumors and UC cell lines and that treatment with TOC at physiologically relevant concentrations has no direct anti-proliferative effect on UC cells.



2019 ◽  
Vol 41 (2) ◽  
pp. 123-129 ◽  
Author(s):  
Takashi Kohno ◽  
Junya Tabata ◽  
Takashi Nakaoku

Abstract RET (REarranged during Transfection), which encodes a receptor tyrosine kinase for members of the glial cell line-derived neurotrophic factor, plays a role as driver oncogene in a variety of human cancers. Fusion of RET with several partner genes has been detected in papillary thyroid, lung, colorectal, pancreatic and breast cancers, and tyrosine kinase inhibitors (TKIs) for RET (particularly RET-specific inhibitors) show promising therapeutic effects against such cancers. Oncogenic mutations within the extracellular cysteine-rich and intracellular kinase domains of RET drive medullary thyroid carcinogenesis; the same mutations are also observed in a small subset of diverse cancers such as lung, colorectal and breast cancers. Considering the oncogenic nature of RET mutants, lung, colorectal and breast cancers are predicted to respond to RET TKIs in a manner similar to medullary thyroid cancer. In summary, cancers carrying oncogenic RET alterations as a driver mutation could be collectively termed ‘REToma’ and treated with RET TKIs in a tissue-agnostic manner.



PLoS ONE ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. e32297 ◽  
Author(s):  
Liza L. Lahaye ◽  
Rene R. Wouda ◽  
Anja W. M. de Jong ◽  
Lee G. Fradkin ◽  
Jasprina N. Noordermeer


2006 ◽  
Vol 66 (18) ◽  
pp. 9162-9170 ◽  
Author(s):  
Jennifer M. O'Toole ◽  
Karen E. Rabenau ◽  
Kerri Burns ◽  
Dan Lu ◽  
Venkat Mangalampalli ◽  
...  


Sign in / Sign up

Export Citation Format

Share Document