Project description:LINC00920 is a tumor-associated lncRNA identified in the transcriptome dataset of the International Cancer Genome Consortium-Early Onset Prostate Cancer (ICGC-EOPC) cohort. SiRNA-mediated knockdown of LINC00920 negatively affected proliferation, colony formation, and migration of PC-3 prostate cancer cells. Genome-wide expression profiling was performed to identify cellular pathways affected by LINC00920.
Project description:In the title compound, C(35)H(30)N(2)O(2), the piperidine ring adopts a chair conformation and the pyrrolidine ring adopts an envelope conformation. The naphthalene ring makes dihedral angles of 24.56 (3) and 36.13 (4)° with the terminal phenyl rings. The dihedral angle between the two terminal phenyl rings is 55.27 (5)°. One of the C atoms in the pyrrolidine ring is disordered over two sites, with a refined occupany ratio of 0.670 (3):0.330 (3). An intra-molecular O-H⋯N hydrogen bond generates an S(6) ring. In the crystal structure, inversion dimers linked by pairs of C-H⋯O hydrogen bonds generate R(2) (2)(18) loops within sheets of mol-ecules lying parallel to the bc plane.
Project description:The title steroid, C(29)H(46)O(4), is a furostene derivative with a C=C double-bond length of 1.353?(3)?Å and an E configuration. The side chain is oriented toward the ? face of the A-E steroidal nucleus and presents a disordered terminal CH(2)-OH group [occupancies for resolved sites are 0.591?(9) and 0.409?(9)]. The methyl group at C20 attached to ring E is also oriented toward the ? face, avoiding steric hindrance with the carbonyl O atom of the acetyl group. The furostene and acetyl functionalities form an ?,?-unsaturated ketone system, with an s-cis configuration. All hydr-oxy and carbonyl groups are involved in weak inter-molecular hydrogen bonds. The absolute configuration was assigned from the synthesis.
Project description:Neonatal inflammatory diseases are associated with severe morbidity, but the inflammatory factors underlying them and their potential effector mechanisms are poorly defined. Here we show that necrotizing enterocolitis in neonate mice is accompanied by elevation of IL-23 and IL-22 and decreased production of pancreatic enzymes. These phenotypes are mirrored in neonate mice overexpressing IL-23 in CX3CR1+ myeloid cells or in keratinocytes. The mice fail to grow and die prematurely, displaying systemic inflammation, nutrient malabsorption and decreased expression of intestinal and pancreatic genes mediating digestion and absorption of carbohydrates, proteins, and lipids. Germ-free environment improves, and genetic ablation of IL-22 restores normal growth in mice overexpressing IL-23. Mechanistically, IL-22 acts directly at the level of pancreatic acinar cells to decrease expression of the pancreas associated transcription factor 1a (PTF1a). These results show that augmented production of IL-23 and IL-22 in early life has a negative impact on pancreatic enzyme secretion and food absorption.