Results 111 to 120 of about 36,550 (274)
This study investigated how PYCR1 inhibition in bone marrow stromal cells (BMSCs) indirectly affects multiple myeloma (MM) cell metabolism and viability. Culturing MM cells in conditioned medium from PYCR1‐silenced BMSCs impaired oxidative phosphorylation and increased sensitivity to bortezomib.
Inge Oudaert +13 more
wiley +1 more source
Some new approaches are described for the synthesis of protein epitope mimetics, in particular, mimics of ?-hairpin structures found in antibodies, growth factors, and other proteins involved in macromolecular recognition in Nature. The mimetics
Luyong Jiang +3 more
doaj
Combinatorial chemistry in toad: a protoxin self-resistance way to its own bufadienolide toxin [PDF]
Denglang Zou +5 more
openalex +1 more source
Following high dose rate brachytherapy (HDR‐BT) for hepatocellular carcinoma (HCC), patients were classified as responders and nonresponders. Post‐therapy serum induced increased BrdU incorporation and Cyclin E expression of Huh7 and HepG2 cells in nonresponders, but decreased levels in responders.
Lukas Salvermoser +14 more
wiley +1 more source
Harnessing natural-product-inspired combinatorial chemistry and computation-guided synthesis to develop N-glycan modulators as anticancer agents. [PDF]
Chen WA +11 more
europepmc +1 more source
Special Issue: Selected Papers from the 2nd International Conference on Natural Products and Physiologically Active Substances (ICNPAS-2004) and the 3rd EuroAsian Heterocyclic Meeting “Heterocycles in Organic and Combinatorial Chemistry” (EAHM-2004) [PDF]
Eugene V. Babaev, Alexey V. Tkachev⊥
openalex +1 more source
Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu +18 more
wiley +1 more source
A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression
Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak +8 more
wiley +1 more source

