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Outputs (25)

Mitochondria form cholesterol-rich contact sites with the nucleus during retrograde response (2020)
Journal Article
Desai, R., East, D. A., Hardy, L., Crosby, J., Faccenda, D., Alvarex, M. S., …Campanella, M. (2020). Mitochondria form cholesterol-rich contact sites with the nucleus during retrograde response. Science Advances, https://doi.org/10.1101/445411

Cholesterol metabolism is pivotal to cellular homeostasis, hormones production, and membranes composition. Its dysregulation associates with malignant reprogramming and therapy resistance. Cholesterol is trafficked into the mitochondria for steroidog... Read More about Mitochondria form cholesterol-rich contact sites with the nucleus during retrograde response.

Dysregulated cell signalling and reduced satellite cell potential in ageing muscle (2019)
Journal Article
Patel, K., Simbi, B. H., Ritvos, O., Vaiyapuri, S., & Dhoot, G. K. (2019). Dysregulated cell signalling and reduced satellite cell potential in ageing muscle. Experimental Cell Research, 385(2), https://doi.org/10.1016/j.yexcr.2019.111685

Aberrant activation of signalling pathways has been postulated to promote age related changes in skeletal muscle. Cell signalling activation requires not only the expression of ligands and receptors but also an appropriate environment that facilitate... Read More about Dysregulated cell signalling and reduced satellite cell potential in ageing muscle.

Dysregulated cancer cell transdifferentiation into erythrocytes is an additional metabolic stress in hepatocellular carcinoma (2018)
Journal Article
Hughes, A., & Dhoot, G. K. (2018). Dysregulated cancer cell transdifferentiation into erythrocytes is an additional metabolic stress in hepatocellular carcinoma. Tumor Biology, 40(11), https://doi.org/10.1177/1010428318811467

A number of human and canine hepatocellular carcinoma tissues showed clear signs of hypoxia indicated by HIF1α-activation and the presence of large clusters of cells resembling erythrocytes at different stages of nuclear elimination without any defin... Read More about Dysregulated cancer cell transdifferentiation into erythrocytes is an additional metabolic stress in hepatocellular carcinoma.

Control of Mitochondrial Remodeling by the ATPase Inhibitory Factor 1 Unveils a Pro-survival Relay via OPA1 (2017)
Journal Article
Faccenda, D., Nakamura, J., Gorini, G., Dhoot, G. K., Piacentini, M., Yoshida, M., & Campanella, M. (2017). Control of Mitochondrial Remodeling by the ATPase Inhibitory Factor 1 Unveils a Pro-survival Relay via OPA1. Cell Reports, https://doi.org/10.1016/j.celrep.2017.01.070

The ubiquitously expressed ATPase inhibitory factor 1 (IF1) is a mitochondrial protein that blocks the reversal of the F1Fo-ATPsynthase, preventing dissipation of cellular ATP and ischemic damage. IF1 suppresses programmed cell death, enhancing tumor... Read More about Control of Mitochondrial Remodeling by the ATPase Inhibitory Factor 1 Unveils a Pro-survival Relay via OPA1.

Short SULF1/SULF2 splice variants predominate in mammary tumours with a potential to facilitate receptor tyrosine kinase-mediated cell signalling (2016)
Journal Article
Gill, R. M. S., Mehra, V., Milford, E., & Dhoot, G. K. (2016). Short SULF1/SULF2 splice variants predominate in mammary tumours with a potential to facilitate receptor tyrosine kinase-mediated cell signalling. Histochemistry and Cell Biology, 146, 431-144. https://doi.org/10.1007/s00418-016-1454-3

The relative roles of SULF1 and SULF2 enzymes in tumour growth are controversial, but short SULF1/SULF2 splice variants predominate in human mammary tumours despite their non-detectable levels in normal mammary tissue. Compared with the normal, the l... Read More about Short SULF1/SULF2 splice variants predominate in mammary tumours with a potential to facilitate receptor tyrosine kinase-mediated cell signalling.

SULF1/SULF2 splice variants differentially regulate pancreatic tumour growth progression.
Journal Article
Gill, R. M. S., Michael, A., Westley, L., Kocher, H. M., Murphy, J. I., & Dhoot, G. K. (in press). SULF1/SULF2 splice variants differentially regulate pancreatic tumour growth progression. Experimental Cell Research, 324, 157-171. https://doi.org/10.1016/j.yexcr.2014.04.001

This study highlights the highly dynamic nature of SULF1/SULF2 splice variants in different human pancreatic cancers that regulate the activities of multiple cell signalling pathways in development and disease. Most pancreatic tumours expressed varia... Read More about SULF1/SULF2 splice variants differentially regulate pancreatic tumour growth progression..