Electro-Conversion of Carbon Dioxide to Valuable Chemicals in a Membrane Electrode Assembly

Electro-conversion of carbon dioxide (CO2) into valuable chemicals is an efficient method to deal with excessive CO2 in the atmosphere. However, undesirable CO2 reaction kinetics in the bulk solution strongly limit current density, and thus it is incompetent in market promotion. Flow cell technology provides an insight into uplifting current density. As an efficient flow cell configuration, membrane electrode assembly (MEA) has been proposed and proven as a viable technology for scalable CO2 electro-conversion, promoting current density to several hundred mA/cm2. In this review, we systematically reviewed recent perspectives and methods to put forward the utilization of state-of-the-art MEA to convert CO2 into valuable chemicals. Configuration design, catalysts nature, and flow media were discussed. At the end of this review, we also presented the current challenges and the potential directions for potent MEA design. We hope this review could offer some clear, timely, and valuable insights on the development of MEA for using wastewater-produced CO2

Electro-Conversion of Carbon Dioxide to Valuable Chemicals in a Membrane Electrode Assembly

Electro-conversion of carbon dioxide (CO2) into valuable chemicals is an efficient method to deal with excessive CO2 in the atmosphere. However, undesirable CO2 reaction kinetics in the bulk solution strongly limit current density, and thus it is incompetent in market promotion. Flow cell technology provides an insight into uplifting current density. As an efficient flow cell configuration, membrane electrode assembly (MEA) has been proposed and proven as a viable technology for scalable CO2 electro-conversion, promoting current density to several hundred mA/cm2. In this review, we systematically reviewed recent perspectives and methods to put forward the utilization of state-of-the-art MEA to convert CO2 into valuable chemicals. Configuration design, catalysts nature, and flow media were discussed. At the end of this review, we also presented the current challenges and the potential directions for potent MEA design. We hope this review could offer some clear, timely, and valuable insights on the development of MEA for using wastewater-produced CO2

The ubiquitin ligase TRAF6 negatively regulates the JAK-STAT signaling pathway by binding to STAT3 and mediating its ubiquitination.

STAT3 is a key transcription factor that mediates various cellular and organismal processes, such as cell growth, apoptosis, immune response and cancer. However, the molecular mechanisms of STAT3 regulation remain poorly understood. Here, we identified TRAF6 as a new STAT3 interactor. TRAF6 augmented the ubiquitination of STAT3 and deactivated its transcriptional activity induced by IFNα stimulation or overexpressed with JAK2. Both the RING domain and the TRAF-type zinc finger domain of TRAF6 were indispensable for STAT3 deactivation. Accordingly, TRAF6 also down-regulated the expression of two known STAT3 target genes, CRP and ACT. Therefore, we showed that TRAF6 is a new regulator of JAK/STAT signaling and provide a new mechanistic explanation for the crosstalk between the NF-κB and the JAK-STAT pathways

Involvement of glycogen synthase kinase-3β in liver ischemic conditioning induced cardioprotection against myocardial ischemia and reperfusion injury in rats

Remote ischemic conditioning has been convincingly shown to render the myocardium resistant to a subsequent more severe sustained episode of ischemia. Compared with other organs, little is known regarding the effect of transient liver ischemic conditioning. We proposed the existence of cardioprotection induced by remote liver conditioning. Male Sprague-Dawley rats were divided into sham-operated control (no further hepatic intervention) and remote liver ischemic conditioning groups. For liver ischemic conditioning, three cycles of 5 min of liver ischemia-reperfusion stimuli were conducted before-(liver preconditioning), post-myocardial ischemia (liver postconditioning), or in combination of both (liver preconditioning + liver postconditioning). Rats were exposed to 45 min of left anterior descending coronary artery occlusion, followed by 3 h of reperfusion thereafter. ECG and hemodynamics were measured throughout the experiment. The coronary artery was reoccluded at the end of reperfusion for infarct size determination. Blood samples were taken for serum lactate dehydrogenase and creatine kinase-MB test. Heart tissues were taken for apoptosis measurements and Western blotting. Our data demonstrate that liver ischemic preconditioning, postconditioning, or a combination of both, offered strong cardioprotection, as evidenced by reduction in infarct size and cardiac tissue damage, recovery of cardiac function, and inhibition of apoptosis after ischemia-reperfusion. Moreover, liver ischemic conditioning increased cardiac (not hepatic) glycogen synthase kinase-3β (GSK-3β) phosphorylation. Accordingly, inhibition of GSK-3β mimicked the cardioprotective action of liver conditioning. These results demonstrate that remote liver ischemic conditioning protected the heart against ischemia and reperfusion injury via GSK-3β-dependent cell-survival signaling pathway.NEW & NOTEWORTHY Remote ischemic conditioning protects hearts against ischemia and reperfusion (I/R) injury. However, it is unclear whether ischemic conditioning of visceral organs such as the liver, the largest metabolic organ in the body, can produce cardioprotection. This is the first study to show the cardioprotective effect of remote liver ischemic conditioning in a rat model of myocardial I/R injury. We also, for the first time, demonstrated these protective properties are associated with glycogen synthase kinase-3β-dependent cell-survival signaling pathway

TRAF6 interacts with STAT3 and mediates the ubiquitination of STAT3.

<p>(A) TRAF6 interacts with STAT3 in mammalian cells. Myc-TRAF6 and Flag-STAT3 were co-transfected into HEK293 cells. After 24 h, the cell lysates were immunoprecipitated with anti-Flag antibody and subjected to Western blot with the anti-Flag or anti-Myc antibodies. (B) The cell lysates of HEK293 cells were immunoprecipitated with anti-TRAF6 antibody and subjected to Western blot with the anti-TRAF6 or anti-STAT3 antibodies. (C) Myc-TRAF6 was transfected into HEK293 cells in a dose-dependent manner. After 24 h, the cell lysates were probed with anti-Myc, anti-STAT3 and anti-GAPDH antibodies. (D, E and F) TRAF6 mediates the ubiquitination of STAT3. HA-Ub(WT) (D), HA-Ub(K63R) (E) or HA-Ub(K48R) (F) and Flag-STAT3 were co-expressed in HEK293 cells with Myc-TRAF6 or empty vectors. The cell lysates and immunoprecipitates were resolved by SDS-PAGE and immunoblotted with anti-HA or anti-Flag antibodies. The data are representative of at least three independent experiments.</p

TRAF6 inhibits the transcriptional activity of STAT3.

<p>(A, B) TRAF6 represses the activity of STAT3 with IFNα stimulation. HEK293 cells were transiently transfected with the indicated combinations of m67 luciferase reporter or 4×IRF luciferase reporter, pRL-TK control, STAT3 and TRAF6. Then the cells were treated with IFNα (50 ng/ml) for 6 h before lysis. After 24 h, the cell lysates were collected for luciferase activity measurements. Data are presented as the means ± S.D. (n = 3). (C, D) TRAF6 inhibits the activity of STAT3 with the forced expression of JAK2. HEK293 cells were transiently transfected with GAS luciferase reporter or m67 luciferase reporter, TRAF6, STAT3 and JAK2. After 24 h, the cell lysates were collected for luciferase activity measurements. Data are presented as the means ± S.D. (n = 3).</p

The RING finger domain and the TRAF-type zinc finger domain play key roles in the regulation of the transcriptional activity of STAT3.

<p>(A) A schematic illustration of TRAF6 domains. The asterisk indicates the expression of TRAF6 mutants that was detected by Western blot with anti-Flag antibody. (B and C) Reporter gene assays of STAT3. HEK293 cells were transiently transfected with various TRAF6 truncated mutants, m67 luciferase plasmids (B) or 4×IRF luciferase plasmids (C), STAT3 and pRL-TK plasmids. After 24 h, the cell lysates were collected for luciferase activity measurements. Data are presented as the means ± S.D. (n = 3).</p

TRAF6 negatively regulates the expression of the STAT3 target genes.

<p>(A) TRAF6 inhibited the expression of the STAT3 target gene, <i>CRP</i>. The HEK293 cells were transfected with the indicated amounts of TRAF6. After 24 h, the HEK293 cells were stimulated with IFNα for 15 min and the mRNA levels of <i>CRP</i> were examined by real-time PCR. The expression values were normalized to the expression of <i>GAPDH</i>. Data are presented as the means ± S.D. (n = 3). (B) TRAF6 inhibited the expression of <i>ACT</i>. HEK293 cells were transiently transfected with the indicated combinations of pACT luciferase reporter, pRL-TK control TRAF6, STAT3 and JAK2. After 24 h, the cell lysates were collected for luciferase activity measurements. Data are presented as the means ± S.D. (n = 3). These results are representative of three independent experiments. (**<i>P</i><0.01 compared with control samples which are not transfected with TRAF6, Student's t test).</p

A Yeast BiFC-seq Method for Genome-wide Interactome Mapping

Genome-wide physical protein–protein interaction (PPI) mapping remains a major challenge for current technologies. Here, we reported a high-efficiency BiFC-seq method, yeast-enhanced green fluorescent protein-based bimolecular fluorescence complementation (yEGFP-BiFC) coupled with next-generation DNA sequencing, for interactome mapping. We first applied yEGFP-BiFC method to systematically investigate an intraviral network of the Ebola virus. Two-thirds (9/14) of known interactions of EBOV were recaptured, and five novel interactions were discovered. Next, we used the BiFC-seq method to map the interactome of the tumor protein p53. We identified 97 interactors of p53, more than three-quarters of which were novel. Furthermore, in a more complex background, we screened potential interactors by pooling two BiFC libraries together and revealed a network of 229 interactions among 205 proteins. These results show that BiFC-seq is a highly sensitive, rapid, and economical method for genome-wide interactome mapping