Results 191 to 200 of about 2,144,828 (297)

Editorial: Forest genomics and biotechnology [PDF]

open access: yes, 2019
Allona, Isabel   +4 more
core   +1 more source

Adaptor protein CIN85 potentiates the motility of osteosarcoma cells via the Akt/mTOR and MMP2‐COL3A1 axis

open access: yesMolecular Oncology, EarlyView.
CIN85 is highly expressed in osteosarcoma, particularly in metastatic lesions. Its overexpression increases cell migration and Matrigel invasion, while silencing CIN85 suppresses these behaviors. Transcriptome analysis shows that CIN85 regulates MMP2, COL3A1, and Akt/mTOR signaling. Targeting these pathways reverses CIN85‐induced motility, highlighting
Iryna Horak   +10 more
wiley   +1 more source

Interaction of HS1BP3 with cortactin modulates TKS5 localisation, cell secretion and cancer malignancy

open access: yesMolecular Oncology, EarlyView.
Here, we demonstrate that HS1BP3 interacts with Cortactin through a proline‐rich region (PRR3.1) and show that this interaction, and HS1BP3 itself, promote cancer cell proliferation and invasion. Inhibition of this interaction leads to build‐up of TKS5 in multivesicular endosomes and altered secretion of CD63 and CD9, providing an explanation for the ...
Arja Arnesen Løchen   +9 more
wiley   +1 more source

Unraveling forensic timelines using molecular markers in Phormia regina maggots. [PDF]

open access: yesPLoS Genet
Lin SH   +4 more
europepmc   +1 more source

Proteasome inhibitor, ixazomib prevents topoisomerase‐I degradation and reverses irinotecan resistance in colorectal cancer

open access: yesMolecular Oncology, EarlyView.
Ixazomib inhibits proteasome‐mediated degradation of topoisomerase I induced by irinotecan, thereby restoring drug sensitivity and promoting tumor cell death in colorectal cancer. Irinotecan, a topoisomerase I (topoI) inhibitor, is widely used for colorectal cancer, but resistance remains a major clinical challenge.
Yuho Ebata   +10 more
wiley   +1 more source

Checkpoint blockade and the stem‐like T cell trade‐off

open access: yesMolecular Oncology, EarlyView.
Stem‐like T cells are key to the success of programmed cell death protein 1 (PD1) blockade, as they sustain long‐term anti‐tumor response by continuously generating effector CD8+ T cells. However, how these cells are maintained in cancer is not fully understood. Hor et al.
Julie M. Mazet, Johanna A. Joyce
wiley   +1 more source

Home - About - Disclaimer - Privacy