Dnm2fl/f PF4-Cre (Dnm2<sup>Plt-/-</sup>) mice specifically lacking dynamin 2 within the platelet lineage developed severe thrombocytopenia and bleeding diathesis and Dnm2Plt platelets adhered poorly to collagen under arterial shear rates.
Dnm2fl/f PF4-Cre (Dnm2<sup>Plt-/-</sup>) mice specifically lacking dynamin 2 within the platelet lineage developed severe thrombocytopenia and bleeding diathesis and Dnm2Plt platelets adhered poorly to collagen under arterial shear rates.
Echocardiography showed left-ventricular hypertrophy in five patients: 2/17 and 3/34 patients with a Dynamin 2 (DNM2) and a RYR1 mutation, respectively.
Increased expression levels of the gene for caveolin, <i>Cav-1</i>, resulting in augmented cellular metastasis and invasion, have been demonstrated in various types of cancer, and overexpression of the gene for dynamin-2, <i>DNM2</i>, has been associated with tumorigenesis in cervical, pancreatic and lung cancer.
Increased expression levels of the gene for caveolin, <i>Cav-1</i>, resulting in augmented cellular metastasis and invasion, have been demonstrated in various types of cancer, and overexpression of the gene for dynamin-2, <i>DNM2</i>, has been associated with tumorigenesis in cervical, pancreatic and lung cancer.
Increased expression levels of the gene for caveolin, <i>Cav-1</i>, resulting in augmented cellular metastasis and invasion, have been demonstrated in various types of cancer, and overexpression of the gene for dynamin-2, <i>DNM2</i>, has been associated with tumorigenesis in cervical, pancreatic and lung cancer.
We propose that DNM2-associated DNA repair enzyme trafficking is important for HDR efficiency and is a powerful predictor of sensitivity to breast cancer chemotherapy and an important target for therapy.
In addition, as recent studies connected <i>AATK</i> and frontotemporal dementia (FTD) and <i>DNM2</i> and hereditary spastic paraplegia (HSP), these two genes together with our results genetically connect, at least in part, five diseases, including FTD, HSP, Charcot-Marie-Tooth (type CMT2M), CNM, and ALS, thus opening future research toward a better understanding of the cell biology involved in these partly overlapping pathologies.
We propose that DNM2-associated DNA repair enzyme trafficking is important for HDR efficiency and is a powerful predictor of sensitivity to breast cancer chemotherapy and an important target for therapy.
In a retrospective analysis, levels of DNM2 at the time of treatment strongly predicted chemotherapy outcome for estrogen receptor-negative and especially for TNBC patients.
Hub genes including CAD, CCND1, ATM, RB1, MET, EGFR, ACTA1, SST, ESR1 and DNM2 might serve as aberrantly methylation-based biomarkers for precise diagnosis and treatment of CRC in the future.
Mutations in Dnm2, a GTPase, are highly disease-specific and have been implicated in four forms of human diseases: centronuclear myopathy, Charcot-Marie Tooth neuropathy and, more recently, T-cell leukaemia and Hereditary Spastic Paraplegia, but red cell abnormalities have not been reported to date.
DNM2 expression was significantly increased in CML stem/progenitor cells; knockdown of DNM2 greatly impaired their survival and sensitized them to TKI treatments.
Dynamin-2 (Dyn2) is implicated in endocytosis of receptor tyrosine kinases, which contribute to hepatic stellate cell (HSC) activation and liver fibrosis.
Even if it is universally accepted that the large GTPase dynamin-2 is important during HIV-1 entry, its exact role during the first steps of HIV-1 infection is not well characterized.