Holmsellers6731

Nonexpressor of pathogenesis-related (NPR) genes are bona fide transcription cofactors in the signal transduction pathway of salicylic acid (SA) and play critical regulatory roles in plant immunity. However, the NPR family genes in Brassica juncea var. tumida have not yet been comprehensively identified and analyzed as of yet. In the present study, NPR genes in B. juncea var. tumida seedlings were identified, and the tissue-specific expression patterns of NPR genes in the seedling were analyzed under salt stress (200 mM) treatment and infection by Plasmodiophora brassicae. A total of 19 NPR family genes clustering into six separate groups were identified in the genome of B. juncea var. tumida. These BjuNPR family genes were located in 11 of 18 chromosomes of B. juncea var. tumida and each possessed 1-5 exons. The BjuNPR family members had similar protein structures and conserved motifs. The BjuNPR genes exhibited tissue-specific expression patterns in the root, stem, leaf, flower and pod. Some BjuNPR genes were sensitive to salt stress and showed up-regulated or down-regulated expression patterns and most BjuNPR genes were up-regulated upon infection by P. brassicae. selleck chemicals This study provides a foundation for further research into BjuNPR genes regulation in plant growth, development, and abiotic stress tolerance.The insulin/insulin-like growth factor signaling (IIS) pathway is well-known in regulation of cell growth and proliferation in vertebrates, while its role in invertebrates such as mollusks remains largely unknown. In this study, we performed an extensive multi-omics data mining and identified four insulin-like peptide genes, including ILP, MIRP3, MIRP3-like and ILP7, in the Pacific oyster, Crassostrea gigas. Their potential roles in growth regulation were further investigated using the selectively bred fast-growing C. gigas variety "Haida No.1". Expression profiling and in situ hybridization of these insulin-like peptides suggested their distinct tissue-specific expression pattern, with dominant expression in the neural enrichment tissues such as labial palp, visceral ganglia, adductor muscle, and digestive gland. The expressions of insulin-like peptides were significantly altered by food abundance in a gene-specific fashion. The expression of ILP was reduced during fasting and increased after re-feeding, the expressions of MIRP3 and ILP7 were generally induced during fasting and down-regulated after re-feeding, while the expression of MIRP3-like was firstly up-regulated and then down-regulated during the fasting and re-feeding process. Furthermore, the expressions of all four insulin-like peptide genes were significantly suppressed at low temperature, in accordance with the growth inhibition. These results indicated that all four insulin-like peptides would play critical but different roles in regulation of growth in the oysters. This work provides valuable information for further investigation on growth regulation mechanism in mollusks and molecular assisted breeding of growth with other production traits in the Pacific oyster.Docetaxel (DTX) is a chemotherapeutic agent used in the treatment of various malignancies but is often associated with central and peripheral neurotoxicity. The aim of this study was to investigate the neuroprotective effect of silymarin (SLM) against DTX-induced central and peripheral neurotoxicities in rats. Rats received 25 and 50 mg/kg body weight SLM orally for seven consecutive days after receiving a single injection of 30 mg/kg body weight DTX on the first day. SLM significantly decreased brain lipid peroxidation level and ameliorated brain glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities in DTX-administered rats. SLM attenuated levels of nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), glial fibrillary acidic protein (GFAP) and activity of p38α mitogen-activated protein kinase (p38α MAPK) whereas caused an increase in levels of neural cell adhesion molecule (NCAM) in the brain and sciatic nerve of DTX-induced rats. In addition, SLM improved the histological structure of the brain and sciatic nerve tissues and decreased the expression of c-Jun N-terminal kinase (JNK) in the sciatic nerve whereas increased cyclic AMP response element binding protein (CREB) expression in the brain induced by DTX. Additionally, SLM markedly up-regulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and B-cell lymphoma-2 (Bcl-2) and downregulated the expression of Bcl-2 associated X protein (Bax) in the brain and sciatic nerve tissues of DTX-induced rats. Our results show that SLM can protect DTX-induced brain and sciatic nerve injuries by enhancing the antioxidant defense system and suppressing apoptosis and inflammation.

Deficiency of folliculin (FLCN) may lead to renal cell carcinoma (RCC) in patients with Birt-Hogg-Dubé (BHD) disease. In this study, we investigated the cytotoxicity induced by PARP inhibitor olaparib in FLCN deficient RCC cells, and the interaction between FLCN and BRCA1 A complex-regulated DNA repair pathway.

FLCN expressing (ACHN and UOK257-F) and FLCN deficient (ACHN-2 and UOK257) cell lines were used in this research. Cell viability was detected by clonogenic assay and MTT assay. Flow cytometry and TUNEL assay were used to detect apoptosis. Autophagy in cells was measured by MDC assay, western blot, and transmission electron microscopy. Co-immunoprecipitation, immunofluorescence and western blot experiments were performed to determine the interaction between FLCN protein and BRCA1 A complex. The in vivo experiments were performed in a xenograft model by inoculating UOK 257 in nude mice.

RCC cells with FLCN protein deficiency were more sensitive to olaparib treatment than the cells with FLCN expression. Olaparib treatment led to more severe autophagy and apoptosis in FLCN deficient ACHN-2 and UOK257 cells compared to the FLCN expressing ACHN and UOK257-F cells. Decreased BRCA1 A complex expression and disruption of DNA repair ability were detected in FLCN-deficient cells, suggesting that FLCN deficiency impaired BRCA1 A complex expression and sensitized cells to PARP inhibitor olaparib.

RCC cells deficient in FLCN are sensitive to olaparib treatment due to the impairment of BRCA1 A complex associated DNA repair ability. The results suggest that PARP inhibitor, such as olaparib, may be a potentially effective therapeutic approach for kidney tumors with deficiency of FLCN protein.

RCC cells deficient in FLCN are sensitive to olaparib treatment due to the impairment of BRCA1 A complex associated DNA repair ability. The results suggest that PARP inhibitor, such as olaparib, may be a potentially effective therapeutic approach for kidney tumors with deficiency of FLCN protein.