All Outputs (5)

Microtubule modification defects underlie cilium degeneration in cell models of retinitis pigmentosa associated with pre-mRNA splicing factor mutations (2022)
Journal Article
Nazlamova, L., Villa Vasquez, S. S., Lord, J., Karthik, V., Cheung, M., Lakowski, J., & Wheway, G. (2022). Microtubule modification defects underlie cilium degeneration in cell models of retinitis pigmentosa associated with pre-mRNA splicing factor mutations. Frontiers in Genetics, 13, 1009430. https://doi.org/10.3389/fgene.2022.1009430

Retinitis pigmentosa (RP) is the most common cause of hereditary blindness, and may occur in isolation as a non-syndromic condition or alongside other features in a syndromic presentation. Biallelic or monoallelic mutations in one of eight genes enco... Read More about Microtubule modification defects underlie cilium degeneration in cell models of retinitis pigmentosa associated with pre-mRNA splicing factor mutations.

WT1 activates transcription of the splice factor kinase SRPK1 gene in PC3 and K562 cancer cells in the absence of corepressor BASP1 (2020)
Journal Article
Belali, T., Wodi, C., Clark, B., Cheung, M. K., Craig, T. J., Wheway, G., …Ladomery, M. (2020). WT1 activates transcription of the splice factor kinase SRPK1 gene in PC3 and K562 cancer cells in the absence of corepressor BASP1. BBA - Gene Regulatory Mechanisms, 1863(12), Article 194642. https://doi.org/10.1016/j.bbagrm.2020.194642

Dysregulated alternative splicing plays a prominent role in all hallmarks of cancer. The splice factor kinase SRPK1 drives the activity of oncogenic splice factors such as SRSF1. SRSF1 in turn promotes the expression of splice isoforms that favour tu... Read More about WT1 activates transcription of the splice factor kinase SRPK1 gene in PC3 and K562 cancer cells in the absence of corepressor BASP1.

The oncogenic transcription factor ERG represses the transcription of the tumour suppressor gene PTEN in prostate cancer cells (2017)
Journal Article
Adamo, P., Porazinski, S., Rajatileka, S., Jumbe, S., Hagen, R., Cheung, M. K., …Ladomery, M. (2017). The oncogenic transcription factor ERG represses the transcription of the tumour suppressor gene PTEN in prostate cancer cells. Oncology Letters, 14(5), 5605-5610. https://doi.org/10.3892/ol.2017.6841

© 2017, Spandidos Publications. All rights reserved. The oncogene ETS-related gene (ERG) encodes a transcription factor with roles in the regulation of haematopoiesis, angiogenesis, vasculogenesis, inflammation, migration and invasion. The ERG oncoge... Read More about The oncogenic transcription factor ERG represses the transcription of the tumour suppressor gene PTEN in prostate cancer cells.

WT1 Mutants Reveal SRPK1 to Be a Downstream Angiogenesis Target by Altering VEGF Splicing (2011)
Journal Article
Bates, D. O., Hinton, D. R., Harper, S. J., Schumacher, V. A., Saleem, M. A., Nowak, D. G., …Ladomery, M. (2011). WT1 Mutants Reveal SRPK1 to Be a Downstream Angiogenesis Target by Altering VEGF Splicing. Cancer Cell, 20(6), 768-780. https://doi.org/10.1016/j.ccr.2011.10.016

Angiogenesis is regulated by the balance of proangiogenic VEGF 165 and antiangiogenic VEGF 165b splice isoforms. Mutations in WT1, the Wilms' tumor suppressor gene, suppress VEGF 165b and cause abnormal gonadogenesis, renal failure, and Wilms' tumors... Read More about WT1 Mutants Reveal SRPK1 to Be a Downstream Angiogenesis Target by Altering VEGF Splicing.

ABA, hydrogen peroxide and nitric oxide signalling in stomatal guard cells (2004)
Journal Article
Desikan, R., Cheung, M., Bright, J., Henson, D., Hancock, J. T., & Neill, S. (2004). ABA, hydrogen peroxide and nitric oxide signalling in stomatal guard cells. Journal of Experimental Botany, 55(395), 205-212

Increased synthesis and redistribution of the phytohormone abscisic acid (ABA) in response to water deficit stress initiates an intricate network of signalling pathways in guard cells leading to stomatal closure. Despite the large number of ABA signa... Read More about ABA, hydrogen peroxide and nitric oxide signalling in stomatal guard cells.