Results 151 to 160 of about 739,130 (263)
Flying Fortress, "Knockout Dropper"
Black and white photograph showing a Boeing Flying Fortress (Knockout Dropper)
core
Structural Control of Stromal-Immune Coupling by COL24A1 Underlies Pregnancy Maintenance. [PDF]
Wu T +12 more
europepmc +1 more source
LUNAR is a liver‐specific long noncoding RNA (lncRNA) that is highly expressed in normal liver but becomes epigenetically silenced in hepatocellular carcinoma through promoter hypermethylation. Loss of LUNAR is associated with NOTCH activation, epithelial–mesenchymal transition, and metastasis, whereas restoring LUNAR restrains metastatic progression ...
Se Ha Jang +9 more
wiley +1 more source
First run knockout experiments in the quasi-free region at CEBAF are ...
BOFFI, SIGFRIDO +2 more
core
Loss of lactate dehydrogenase A disrupts R-loop homeostasis and induces DNA damage in breast cancer cells. [PDF]
Li S, Xu C, Chen S, Yin G, Yang D.
europepmc +1 more source
PANoptosis in the pathogenesis of myelodysplastic syndromes
PANoptosis, a combination of three types of programmed cell death, is mediated by a large protein complex called a PANoptosome. In healthy bone marrow hematopoietic cells, PANoptosis is restricted by inhibitory signaling. In MDS, bone marrow cells become sensitive to the PANoptotic stimuli due to the aberrant inactivation of inhibitory signaling or ...
Rohit Thalla +4 more
wiley +1 more source
CD112 Lactylation Drives Dual Immune Evasion From CD8+ T Cells and NK Cells. [PDF]
Xu Z +6 more
europepmc +1 more source
This study identifies somatostatin receptor 4 (Sstr4) as a critical tumor suppressor against skin and head/neck cancers (HNSCC, cSCC, and BCC). The loss of Sstr4 removes a check on cell growth, causing hyperactivation of the MAPK‐ERK signaling pathway (↑).
Ali Taqvi +6 more
wiley +1 more source
A genome-wide CRISPR knockout screen identified host genes essential for Brucella invasion and intracellular survival. [PDF]
Wang X +5 more
europepmc +1 more source
Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim +7 more
wiley +1 more source

