A facile, one-pot reaction cascade condenses 1,1,1-trichloroalkanes with alpha,beta-unsaturated ketones to unexpectedly furnish moderate to good yields of (E)-2-alkylidenecyclobutanols.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2764278PMC
http://dx.doi.org/10.1021/ol901985cDOI Listing

Publication Analysis

Top Keywords

cascade synthesis
4
synthesis e-2-alkylidenecyclobutanols
4
e-2-alkylidenecyclobutanols facile
4
facile one-pot
4
one-pot reaction
4
reaction cascade
4
cascade condenses
4
condenses 111-trichloroalkanes
4
111-trichloroalkanes alphabeta-unsaturated
4
alphabeta-unsaturated ketones
4

Similar Publications

Acute B-lymphoblastic leukemia (B-ALL) is a highly heterogeneous hematologic malignancy, characterized by significant molecular differences among patients as the disease progresses. While the PI3K-Akt signaling pathway and metabolic reprogramming are known to play crucial roles in B-ALL, the interactions between lipid metabolism, immune pathways, and drug resistance remain unclear. In this study, we performed multi-omics analysis on different patient cohorts (newly diagnosed, relapsed, standard-risk, and poor-risk) to investigate the molecular characteristics associated with metabolism, signaling pathways, and immune regulation in B-ALL.

View Article and Find Full Text PDF

Aedes mosquitoes transmit pathogenic arthropod-borne (arbo) viruses, putting nearly half the world's population at risk. Blocking virus replication in mosquitoes is a promising approach to prevent arbovirus transmission, the development of which requires in-depth knowledge of virus-host interactions and mosquito immunity. By integrating multi-omics data, we find that heat shock factor 1 (Hsf1) regulates eight small heat shock protein (sHsp) genes within one topologically associated domain in the genome of the Aedes aegypti mosquito.

View Article and Find Full Text PDF

The role of Box A of HMGB1 in producing γH2AX associated DNA breaks in lung cancer.

Sci Rep

January 2025

Center of Excellence in Molecular Genetics of Cancer and Human Diseases, Department of Anatomy, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial Hospital, Bangkok, Thailand.

An ideal chemotherapeutic agent damages DNA, specifically in cancer cells, without harming normal cells. Recently, we used Box A of HMGB1 plasmid as molecular scissors to produce DNA gaps in normal cells. The DNA gap relieves DNA tension and increases DNA strength, preventing DNA double-strand breaks (DSBs).

View Article and Find Full Text PDF

MarR family regulator LcbR2 activates lincomycin biosynthesis in multiple ways.

Int J Biol Macromol

January 2025

Department of Applied Biology, School of Biotechnology, East China University of Science and Technology, Shanghai 200237, China.

Lincomycin, produced by the actinomycete Streptomyces lincolnensis, is highly effective against Gram-positive bacteria and protozoans, making it widely used in clinical settings. This study identified LcbR2, a MarR family transcriptional regulator, as an activator of lincomycin biosynthesis. Knocking out the lcbR2 gene reduced lincomycin production by 63.

View Article and Find Full Text PDF

Two Cysteines in Raf Kinase Inhibitor Protein Make Differential Contributions to Structural Dynamics In Vitro.

Molecules

January 2025

Cancer Microenvironment Branch, Division of Cancer Biology, Research Institute, National Cancer Center, Goyang-si 10408, Republic of Korea.

As a scaffolding protein, Raf kinase binding protein (RKIP) is involved in a variety of cellular pathways, including the Raf-MEK-ERK-cascade. It acts as a negative regulator by binding to its partners, making it an attractive target in the development of therapeutic strategies for cancer. Despite its structural stability as a monomer, RKIP may form a dimer, resulting in the switching of binding partners.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!