Anti-TUBA1B (full length) polyclonal antibody

We studied the effect of oral administration of metallic silver nanoparticles to rats on the proteome of the liver microsomal fraction. Nanoparticles (5-80 nm) were administered daily to growing Wistar male rats over 92 days. Controls received pure water. To control the effect of the carrier, the rats were administered aqueous solution of a stabilizer polyvinylpyrrolidone. The protein composition (proteome) of the liver microsomal fraction was analyzed by 2D-electrophoresis with identification of variable protein spots using the high-resolution nanoHPLC-MS/MS. Eight, 6, and 8 proteins absent in the control groups appeared in the microsomal fraction under the action of nanoparticles in doses of 0.1, 1, and 10 mg/kg body weight, among these, proteasome activator complex subunit 1 (Psme1 gene), and the heat shock protein HSP60 (Hspd1 gene) were reliably identified. The consumption of silver nanoparticles led to disappearance of protein of 2a tubulin chain (Tuba1b gene) from the microsomal fraction. The expression of catalase, present in the proteome of the liver microsomal fraction in animals of all groups was significantly decreased after consumption of silver nanoparticles in doses of 0.1 and 10 mg/kg. The observed changes in the proteome are considered as manifestations of hepatotoxicity of silver nanoparticles and can be related to the antagonistic effect of silver on the status of the essential trace element selenium.

Nitidine chloride (NC) has been demonstrated to have an anticancer effect in hepatocellular carcinoma (HCC). However, the mechanism of action of NC against HCC remains largely unclear. In this study, three pairs of NC-treated and NC-untreated HCC xenograft tumour tissues were collected for circRNA sequencing analysis. In total, 297 circRNAs were differently expressed between the two groups, with 188 upregulated and 109 downregulated, among which hsa_circ_0088364 and hsa_circ_0090049 were validated by real-time quantitative polymerase chain reaction. The in vitro experiments showed that the two circRNAs inhibited the malignant biological behaviour of HCC, suggesting that they may play important roles in the development of HCC. To elucidate whether the two circRNAs function as "miRNA sponges" in HCC, we identified circRNA-miRNA and miRNA-mRNA interactions by using the CircInteractome and miRwalk, respectively. Subsequently, 857 miRNA-associated differently expressed genes in HCC were selected for weighted gene co-expression network analysis. Module Eigengene turquoise with 423 genes was found to be significantly related to the survival time, pathology grade and TNM stage of HCC patients. Gene functional enrichment analysis showed that the 423 genes mainly functioned in DNA replication- and cell cycle-related biological processes and signalling cascades. Eighteen hubgenes (SMARCD1, CBX1, HCFC1, RBM12B, RCC2, NUP205, ECT2, PRIM2, RBM28, COPS7B, PRRC2A, GPR107, ANKRD52, TUBA1B, ATXN7L3, FUS, MCM8 and RACGAP1) associated with clinical outcomes of HCC patients were then identified. These findings showed that the crosstalk between hsa_circ_0088364 and hsa_circ_0090049 and their competing mRNAs may play important roles in HCC, providing interesting clues into the potential of circRNAs as therapeutic targets of NC in HCC.