TGFBR3 supports anoikis through suppressing ATF4 signaling.

Epithelial morphogenesis and oncogenic transformation can cause loss of cell adhesion, and detached cells are eliminated by anoikis. Here, we reveal that transforming growth factor β receptor 3 (TGFBR3) acts as an anoikis mediator through the coordination of activating transcription factor 4 (ATF4). In breast cancer tissues, TGFBR3 is progressively lost, but elevated TGFBR3 is associated with a histologic subtype characterized by cellular adhesion defects.

Corrigendum to "TERT and Akt Are Involved in the Par-4-Dependent Apoptosis of Islet Cells in Type 2 Diabetes".

[This corrects the article DOI: 10.1155/2018/7653904.].

TERT and Akt Are Involved in the Par-4-Dependent Apoptosis of Islet Cells in Type 2 Diabetes.

Islet cell apoptosis plays an important role in type 2 diabetes. We previously reported that Par-4-mediated islet cell apoptosis is induced by high-glucose/fatty acid levels. In the present study, we show that Par-4, which is induced by high-glucose/fatty acid levels, interacts with and inhibits TERT in the cytoplasm and then translocates to the nucleus.

Dapper1 attenuates hepatic gluconeogenesis and lipogenesis by activating PI3K/Akt signaling.

Studies have shown that hepatic insulin resistance, a disorder of glucose and lipid metabolism, plays a vital role in type 2 diabetes (T2D). To clarify the function of Dapper1 in glucose and lipid metabolism in the liver, we investigated the relationships between Dapper1 and adenosine triphosphate (ATP)- and Ca-mediated activation of PI3K/Akt. We observed a reduction in hepatic Dapper1 in db/db (mice that are homozygous for a spontaneous diabetes mutation) and HFD-induced diabetic mice with T2D.

Exenatide Activates the APPL1-AMPK-PPARα Axis to Prevent Diabetic Cardiomyocyte Apoptosis.

Objective: To investigate the effect and mechanism of the exenatide on diabetic cardiomyopathy.

Methods: Rats were divided into control group, diabetes group (D), diabetes treated with insulin (DI) group, and diabetes treat with exenatide (DE) group. We detected apoptosis rate by TUNEL, the adiponectin and high molecular weight adiponectin (HMW-adiponectin) by ELISA, and the expression of APPL1, p-AMPK/T-AMPK, PPARα, and NF-κB by immunohistochemistry and western blotting.

[Subcellular localization of human endothelial-overexpressed lipopolysaccharide-associated factor 1 protein].

Objective: To study the subcellular localization of human endothelial-overexpressed lipopolysaccharide-associated factor 1 (EOLA1) protein in endothelial cells.

Methods: Human umbilical vein endothelial cell strain ECV304 were cultured in vitro. The fusion protein of enhanced green fluorescent protein (EGFP)-EOLA1 expressing plasmid was constructed.

[The effect of inhibiting EOLA1 expression in ECV304 cells].

Objective: To study the effect of inhibiting the expression of endothelial-overexpressed lipopolysaccharide-associated factor 1 (EOLA1) on proliferation of human umbilical vein endothelial cell line ECV304.

Methods: After constructing and transfecting EGFP-EOLA1 fusion protein expressive vector into ECV304 cells, the transfected cells was cultured in M199 containing G418 for 5 weeks to screen the cell line stable expression EGFP-EOLA1 fusion protein. Oligonucleotides targeting EOLA1 at different sites were synthesized and inserted into pSinencer3.

[Purification of human endothelial overexpressed lipopolysaccharide-associated factor 1 protein].

Objective: To investigate the feasibility of obtaining of a highly pure protein of human endothelial overexpressed lipopolysaccharide-associated factor 1 (EOLA1) with metal chelation chromatography.

Methods: Inclusion bodies of the E. coli transformed with EOLA1 gene were extracted and washed with BugBuster Protein Extraction Reagent.

[Identification and characterization of a novel gene EOLA1 stimulating ECV304 cell proliferation].

Objective: To amplify the full-length cDNA and characterize the structure and biological function of a novel expression sequence tag ST55 (GenBank Accession No. BM121646).

Methods: Rapid amplification of cDNA ends was used to clone the full-length of cDNA of ST55 in this study.

[Establishment of human endothelial-overexpressed lipopolysaccharide-associated factor 1 compelling expression model and its effects on the proliferation of ECV304 cells].

Objective: To design and construct the inducible expression vector of endothelial-overexpressed lipopolysaccharide-associated factor 1 (EOLA1), in order to establish EOLA1 compelling expression model, and to observe the effects of EOLA1 compelling expression on the proliferation of ECV304 cells.

Methods: Inducible overexpression vector pOPRSV I-EOLA1 was constructed by amplifying the open reading fragment of EOLA1 and subcloning it into the Not I site and Xho I site of pOPRSV I vector. After sequencing, the pOPRSV I-EOLA1 recombinant vector and pCMVLac I vector were co-transfected into ECV304 cells.

Cloning of differentially expressed genes following lipopolysaccharide stimulation in human umbilical vein endothelial cells.

Objective: To clone the differentially expressed genes in human umbilical vein endothelial cells (HUVEC) stimulated by lipopolysaccharide (LPS).

Methods: Two-directional (forward and backward) suppression subtractive hybridization (SSH) was performed on HUVEC cultured in either standard media or treated for 6 hours with LPS (100 ng/ml). To restrict the number of false-positive clones, colony dot hybridization was used to further verify the differentially expressed cDNA clones.