ArticleMolecular and cellular biology1989
Mechanism of activation of the human trk oncogene.
Article in Molecular and cellular biology, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 42 citations in OpenAlex.
- Selective type II TRK inhibitors overcome xDFG mutation mediated acquired resistance to the second-generation inhibitors selitrectinib and repotrectinib.Acta pharmaceutica Sinica. B · 2024Review
- Phase separation underlies signaling activation of oncogenic NTRK fusions.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Non-small-cell lung cancer: how to manageDrugs in context · 2022Review
- Discovery of a rareCancer biology & therapy · 2021Article
- Kinase gene fusions: roles and therapeutic value in progressive and refractory papillary thyroid cancer.Journal of cancer research and clinical oncology · 2021Review
- Successful treatment of lipofibromatosis-like neural tumor of the lumbar spine with an NTRK-fusion inhibitor.Clinical sarcoma research · 2020Article
- NTRK fusion-positive cancers and TRK inhibitor therapy.Nature reviews. Clinical oncology · 2018Review
- Novel transcripts reveal a complex structure of the human TRKA gene and imply the presence of multiple protein isoforms.BMC neuroscience · 2015Article
- Novel ALK inhibitors in clinical use and development.Journal of hematology & oncology · 2015Review
- Article
- Inference of cancer-specific gene regulatory networks using soft computing rules.Gene regulation and systems biology · 2010Article
- Kinase expression and chromosomal rearrangements in papillary thyroid cancer tissues: investigations at the molecular and microscopic levels.Journal of physiology and pharmacology : an official journal of the Polish Physiological Society · 2009Article
- BAC-FISH assays delineate complex chromosomal rearrangements in a case of post-Chernobyl childhood thyroid cancer.Folia histochemica et cytobiologica · 2009Article
- Loss of expression of tropomyosin-1, a novel class II tumor suppressor that induces anoikis, in primary breast tumors.Oncogene · 2003Article
- Externalization of tropomyosin isoform 5 in colon epithelial cells.Clinical and experimental immunology · 1999Article
- Transforming activity of retroviral genomes encoding Gag-Axl fusion proteins.Journal of virology · 1996Article
- Dimerization mediated through a leucine zipper activates the oncogenic potential of the met receptor tyrosine kinase.Molecular and cellular biology · 1993Article
- BCR first exon sequences specifically activate the BCR/ABL tyrosine kinase oncogene of Philadelphia chromosome-positive human leukemias.Molecular and cellular biology · 1991Article
- Human trk oncogenes activated by point mutation, in-frame deletion, and duplication of the tyrosine kinase domain.Molecular and cellular biology · 1990Article
- Oncogenic activation of the human trk proto-oncogene by recombination with the ribosomal large subunit protein L7a.The EMBO journal · 1990Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The human trk oncogene was generated by a genetic rearrangement that replaced the extracellular domain of the normal trk tyrosine kinase receptor by sequences coding for the 221 amino-terminal residues of a nonmuscle tropomyosin. Molecular dissection of a cDNA clone of the trk oncogene indicated that both the tropomyosin and tyrosine kinase domains were required for proper transforming activity. Replacement of nonmuscle tropomyosin sequences with those of other tropomyosin isoforms had no deleterious effect. However, when tropomyosin sequences were replaced with those of another cytoskeletal gene, such as beta-actin or beta-globin, transforming activity was completely abolished. These results illustrate the important role of tropomyosin sequences in endowing the trk kinase with transforming properties. Functionally unrelated subdomains of the tropomyosin molecule were equally efficient in activating the trk gene. Moreover, the transforming activity of the trk oncogene was not affected when its subcellular localization was drastically altered. Therefore, tropomyosin sequences are likely to contribute to the malignant activation of the trk oncogene not by facilitating its interaction with defined cytoskeletal structures as initially suspected, but by allowing its kinase domain to fold into a constitutively active configuration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.