Rabbit Anti-Human TKT Polyclonal Antibody Knockout Validated

Obesity has recently become a prevalent health threat worldwide. Although emerging evidence has suggested a strong link between the pentose phosphate pathway (PPP) and obesity, the role of transketolase (TKT), an enzyme in the nonoxidative branch of the PPP that connects PPP and glycolysis, remains obscure in adipose tissues. In this study, we specifically deleted TKT in mouse adipocytes and found no obvious phenotype upon normal diet feeding. However, adipocyte TKT abrogation attenuated high-fat diet-induced obesity, reduced hepatic steatosis, improved glucose tolerance, alleviated insulin resistance, and increased energy expenditure. Mechanistically, TKT deficiency accumulated nonoxidative PPP metabolites and decreased glycolysis and pyruvate input into the mitochondria, leading to increased lipolytic enzyme gene expression and enhanced lipolysis, fatty acid oxidation, and mitochondrial respiration. Therefore, our data not only identify a novel role of TKT in regulating lipolysis and obesity but also suggest that limiting glucose-derived carbon into the mitochondria induces lipid catabolism and energy expenditure.

Transketolase genes are key rate-limiting enzymes in the non-oxidative part of the pentose phosphate pathway, which is an important metabolic pathway in ribose-5-phosphate production. Three human transketolase genes have been identified: Transketolase (TKT), transketolase-like gene 1 (TKTL1) and transketolase-like gene 2 (TKTL2). Transketolase genes serve crucial roles in the tumorigenesis, metastasis and outcome of multiple types of cancer. However, the expression levels and prognostic values of transketolase family genes in patients with ovarian cancer remain unclear. The purpose of the study was to analyze the expression level and prognostic significance of transketolase family genes in ovarian cancer. In the present study, the mRNA expression levels of three transketolase genes in ovarian cancer and normal ovarian tissue were compared by Oncomine. The prognostic values of these genes were systemically assessed using the Kaplan-Meier plotter database. In addition, the associations between the mRNA levels of these transketolase genes and the clinicopathological characteristics of patients with ovarian cancer, such as histological subtype, clinical stage, grade, tumor protein p53 (TP53) mutation status and chemotherapy history were studied. The prognostic roles of transketolase genes were also evaluated in a validation dataset. The results demonstrated that TKT and TKTL1 expression in ovarian cancer tissues was elevated compared with that in normal ovarian tissues. In addition, high mRNA expression of the three transketolase genes was identified to be associated with poorer progression-free survival (PFS) in patients with serous ovarian cancer, especially in patients at an advanced stage. TKTL2 was significantly associated with poor overall survival in all patients with ovarian cancer. Additionally, transketolase family genes served a role in predicting PFS in patients with ovarian cancer treated with platinum and/or taxol. High expression of the three transketolase genes was associated with unfavorable PFS in patients with TP53-mutated ovarian cancer, but not in patients with TP53 wild-type ovarian cancer. These results suggested that transketolase family genes may serve important roles in the prognosis of patients with ovarian cancer.