Project description:Chemostat evolution experiment C1 under glucose-limited condition at 30C. Gene Expression profiles of adaptive clones M1-M5 in evolved conditions compared with original parents. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Genotype: Evolved clones. The genotype is not necessarily complete. Keywords: all_pairs Gene Expression profiles of adaptive clones M1-M5 in evolved conditions compared with original parents
Project description:Chemostat evolution experiment C1 under glucose-limited condition at 30C. Gene Expression profiles of adaptive clones M1-M5 in evolved conditions compared with original parents. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Genotype: Evolved clones. The genotype is not necessarily complete. Keywords: all_pairs
Project description:The aim of this project was to explore the role of muscarinic receptors (M1, M3, and M5) in spermatogenesis. The lentivirus with the knockdown of M1, M3, M5 were injected into mouse testes. Then the testes were collected. The RNA was used for the RNA-seq analysis to search the role of these receptors in the spermatogenesis.
Project description:Unbalanced chromosomal abnormalities might play a major role in the leukemogenesis of AML-M5 Oligonucelotide array CGH were performed on 24 patients with AML-M5
Project description:Unbalanced chromosomal abnormalities might play a major role in the leukemogenesis of AML-M5 Oligonucelotide array CGH were performed on 24 patients with AML-M5 To assess the possible existence of unbalanced chromosomal abnormalities and delineate the characterization of copy number alterations (CNAs) of acute myeloid leukemia-M5 (AML-M5)
Project description:Muscarinic acetylcholine receptor M3 (M3) and its downstream effector Gq/11 are critical drug development targets given their involvement in numerous physiological processes and diseases. Although a cryo-electron microscopy study previously defined the structure of the M3-miniGq complex, the lack of information on the intracellular loop 3 (ICL3) of M3 and α-helical domain (AHD) of Gαq has made it difficult to comprehend the molecular mechanism of M3-Gq coupling fully. Here, we present the molecular mechanism underlying the dynamic interactions between the wild-type full-length M3 and heterotrimeric Gq using hydrogen-deuterium exchange mass spectrometry and NanoLuc Binary Technology-based cell systems. This study suggests potential binding interfaces between M3 and Gq in pre-assembled and fully active nucleotide-free complexes. In addition to well-known binding interfaces, we observed the interaction of long ICL3 with Gβγ. Furthermore, M3 ICL3 negatively affected M3-Gq coupling, and the Gαq AHD underwent unique conformational changes during M3-Gq coupling. Therefore, we propose a comprehensive molecular mechanism of M3-Gq coupling by analyzing previously well-defined binding interfaces and neglected regions, such as M3 ICL3 and the Gαq AHD.
Project description:The goat of this project is to explore M5 receptor regulation spermatogenesis. We tried to search the mechanism of M5 receptor regulation spermatogenesis. RNA-seq of C18-4 and TM4 cells samples from different groups: C3NC, M5 knockdown in C18-4, TM3NC, M5 knockdown in TM4 cells. The cell were transfected with virus with inhibition of M5 expression ( M5 gene knockdown).