This paper explores effective hedging instruments for carbon market risk. Examining the relationship between the carbon futures returns and the returns of four major market indices, i.e., the VIX ...index, the commodity index, the energy index and the green bond index, we find that the connectedness between the carbon futures returns and the green bond index returns is the highest and this connectedness is extremely pronounced during the market's volatile period. Further, we develop and evaluate hedging strategies based on three dynamic hedge ratio models (DCC-APGARCH, DCC-T-GARCH, and DCC-GJR-GARCH models) and the constant hedge ratio model (OLS model). Empirical results show that among the four market indices the green bond index is the best hedge for carbon futures and performs well even in the crisis period. The paper also provides evidence that the dynamic hedge ratio models are superior to the OLS model in the volatile period as more sophisticated models can capture the dynamic correlation and volatility spillover between the carbon futures and market index returns.
•We examine the effectiveness of four major market indices in hedging carbon market risk.•We employ both dynamic and constant hedge ratio models in our analysis.•We find that the green bond index is the most effective and inexpensive hedge for carbon market risk.•We show that the dynamic hedge ratio models are superior in the market's volatile period.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Protein palmitoylation, in which C16 fatty acid chains are attached to cysteine residues via a reversible thioester linkage, is one of the most common lipid modifications and plays important roles in ...regulating protein stability, subcellular localization, membrane trafficking, interactions with effector proteins, enzymatic activity, and a variety of other cellular processes. Moreover, the unique reversibility of palmitoylation allows proteins to be rapidly shuttled between biological membranes and cytoplasmic substrates in a process usually controlled by a member of the DHHC family of protein palmitoyl transferases (PATs). Notably, mutations in PATs are closely related to a variety of human diseases, such as cancer, neurological disorders, and immune deficiency conditions. In addition to PATs, intracellular palmitoylation dynamics are also regulated by the interplay between distinct posttranslational modifications, including ubiquitination and phosphorylation. Understanding the specific mechanisms of palmitoylation may reveal novel potential therapeutic targets for many human diseases.
Protein can be palmitoylated in golgi apparatus by the DHHC‐family, which add a molecule of palmitic acid to the protein. The palmitoylated proteins would traffic to PM via either vesicular transport or diffusion, and then generally translocate to lipid rafts; depalmitoylation is catalyzed by either APT in cytoplasm or PPT1/2 in lysosome, and the depalmitoylated protein would diffuses back to the Golgi complex where it can be palmitoylated for another cycle.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Two new near-infrared (NIR) photochromic compounds, containing both electron-donating (D) and accepting groups (A), have been developed and their NIR photochromic and fluorescence performances can be ...modulated by the cyanide anion. Such a colorimetric cyanide sensor has been achieved based on this donor-photochromic bridge-acceptor system.
The transcription factor BACH1 (BTB and CNC homology 1) suppressed endothelial cells (ECs) proliferation and migration and impaired angiogenesis in the ischemic hindlimbs of adult mice. However, the ...role and underlying mechanisms of BACH1 in atherosclerosis remain unclear.
Mouse models of atherosclerosis in endothelial cell (EC)-specific-Bach1 knockout mice were used to study the role of BACH1 in the regulation of atherogenesis and the underlying mechanisms.
Genetic analyses revealed that coronary artery disease-associated risk variant rs2832227 was associated with BACH1 gene expression in carotid plaques from patients. BACH1 was upregulated in ECs of human and mouse atherosclerotic plaques. Endothelial Bach1 deficiency decreased turbulent blood flow- or western diet-induced atherosclerotic lesions, macrophage content in plaques, expression of endothelial adhesion molecules (ICAM1 intercellular cell adhesion molecule-1 and VCAM1 vascular cell adhesion molecule-1), and reduced plasma TNF-α (tumor necrosis factor-α) and IL-1β levels in atherosclerotic mice. BACH1 deletion or knockdown inhibited monocyte-endothelial adhesion and reduced oscillatory shear stress or TNF-α-mediated induction of endothelial adhesion molecules and/or proinflammatory cytokines in mouse ECs, human umbilical vein ECs, and human aortic ECs. Mechanistic studies showed that upon oscillatory shear stress or TNF-α stimulation, BACH1 and YAP (yes-associated protein) were induced and translocated into the nucleus in ECs. BACH1 upregulated YAP expression by binding to the YAP promoter. BACH1 formed a complex with YAP inducing the transcription of adhesion molecules. YAP overexpression in ECs counteracted the antiatherosclerotic effect mediated by Bach1-deletion in mice. Rosuvastatin inhibited BACH1 expression by upregulating microRNA let-7a in ECs, and decreased Bach1 expression in the vascular endothelium of hyperlipidemic mice. BACH1 was colocalized with YAP, and the expression of BACH1 was positively correlated with YAP and proinflammatory genes, as well as adhesion molecules in human atherosclerotic plaques.
These data identify BACH1 as a mechanosensor of hemodynamic stress and reveal that the BACH1-YAP transcriptional network is essential to vascular inflammation and atherogenesis. BACH1 shows potential as a novel therapeutic target in atherosclerosis.
Hepatic insulin resistance is central to the metabolic syndrome. Here we investigate the role of BTB and CNC homology 1 (BACH1) in hepatic insulin signaling. BACH1 is elevated in the hepatocytes of ...individuals with obesity and patients with non-alcoholic fatty liver disease (NAFLD). Hepatocyte-specific Bach1 deletion in male mice on a high-fat diet (HFD) ameliorates hyperglycemia and insulin resistance, improves glucose homeostasis, and protects against steatosis, whereas hepatic overexpression of Bach1 in male mice leads to the opposite phenotype. BACH1 directly interacts with the protein-tyrosine phosphatase 1B (PTP1B) and the insulin receptor β (IR-β), and loss of BACH1 reduces the interaction between PTP1B and IR-β upon insulin stimulation and enhances insulin signaling in hepatocytes. Inhibition of PTP1B significantly attenuates BACH1-mediated suppression of insulin signaling in HFD-fed male mice. Hepatic BACH1 knockdown ameliorates hyperglycemia and improves insulin sensitivity in diabetic male mice. These results demonstrate a critical function for hepatic BACH1 in the regulation of insulin signaling and glucose homeostasis.
Facing the challenge of resource and environmental constraints, China has been adopted green development as the national strategy for pursuing sustainable long-term target at the stage of rapid ...industrialization, which naturally promotes green finance. The considerable growth in green investment within China has motivated intense debate on the implications of incorporating financial performance and green criteria into the portfolio selection process. However, few literature studies newly-emerged green funds' performance. This article tackles the financial performance of China green funds as well as analyzing the allocation difference across industries of green funds. We find that the performance of China green funds is sensitive to the market factor, small cap and value stocks for the full period. In contrast, after entering the new normal period, China green funds have not been sensitive to the market index, only to value stocks. Green funds play an important role in supporting the main direction of Chinese industrial restructuring and upgrading for the purpose of gaining new competitiveness in the markets. The study finds also that green funds exhibit different industry betas consistent with different portfolio positions. At the individual fund level, green funds have a high weight on manufacturing industries, which shows that China green funds have a characteristic of industry concentration instead of diversification; and steadily confirms that green funds' industry preference has a positive correlation with innovation indicators, indicating that innovation and R&D activities of enterprises are driving the new economy. Especially, the percentage of new intelligent manufacturing has an increasing trend in the new normal. Our findings suggest that green funds can work as a financial power to promote green technological innovation for industries, and to benefit small and medium-sized enterprises with new smart and green technologies.
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•We investigate the financial performance of all China green funds and the industry allocation differences.•The performance of all China green funds is more exposed to small cap and value stocks.•China green funds focus on manufacturing industries.•The percentage of new intelligent manufacturing has an increasing trend in the new normal.•Green funds industry allocation does take fully account of innovation in the new normal.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
The public's health is gravely at risk due to the current global outbreak of emerging viruses, specifically SARS-CoV-2 and MPXV. Recent studies have shown that SARS-CoV-2 mutants (such as Omicron) ...exhibit a higher capability to antagonize the host innate immunity, increasing their human adaptability and transmissibility. Furthermore, current studies on the strategies for MPXV to antagonize the host innate immunity are still in the initial stages. These multiple threats from emerging viruses make it urgent to study emerging virus-host interactions, especially the viral antagonism of host antiviral innate immunity. Given this, we selected several representative viruses that significantly threatened human public health and interpreted the multiple strategies for these viruses to antagonize the host antiviral innate immunity, hoping to provide ideas for molecular mechanism research that emerging viruses antagonize the host antiviral innate immunity and accelerate the research progress. The IAV, SARS-CoV-2, SARS-CoV, MERS-CoV, EBOV, DENV, ZIKV, and HIV are some of the typical viruses. Studies have shown that viruses could antagonize the host antiviral innate immunity by directly or indirectly blocking antiviral innate immune signaling pathways. Proviral host factors, host restriction factors, and ncRNAs (microRNAs, lncRNAs, circRNAs, and vtRNAs) are essential in indirectly blocking antiviral innate immune signaling pathways. Furthermore, via controlling apoptosis, ER stress, stress granule formation, and metabolic pathways, viruses may antagonize it. These regulatory mechanisms include transcriptional regulation, post-translational regulation, preventing complex formation, impeding nuclear translocation, cleavage, degradation, and epigenetic regulation.The public's health is gravely at risk due to the current global outbreak of emerging viruses, specifically SARS-CoV-2 and MPXV. Recent studies have shown that SARS-CoV-2 mutants (such as Omicron) exhibit a higher capability to antagonize the host innate immunity, increasing their human adaptability and transmissibility. Furthermore, current studies on the strategies for MPXV to antagonize the host innate immunity are still in the initial stages. These multiple threats from emerging viruses make it urgent to study emerging virus-host interactions, especially the viral antagonism of host antiviral innate immunity. Given this, we selected several representative viruses that significantly threatened human public health and interpreted the multiple strategies for these viruses to antagonize the host antiviral innate immunity, hoping to provide ideas for molecular mechanism research that emerging viruses antagonize the host antiviral innate immunity and accelerate the research progress. The IAV, SARS-CoV-2, SARS-CoV, MERS-CoV, EBOV, DENV, ZIKV, and HIV are some of the typical viruses. Studies have shown that viruses could antagonize the host antiviral innate immunity by directly or indirectly blocking antiviral innate immune signaling pathways. Proviral host factors, host restriction factors, and ncRNAs (microRNAs, lncRNAs, circRNAs, and vtRNAs) are essential in indirectly blocking antiviral innate immune signaling pathways. Furthermore, via controlling apoptosis, ER stress, stress granule formation, and metabolic pathways, viruses may antagonize it. These regulatory mechanisms include transcriptional regulation, post-translational regulation, preventing complex formation, impeding nuclear translocation, cleavage, degradation, and epigenetic regulation.
The role of BACH1 in the process of vascular smooth muscle cell (VSMC) differentiation from human embryonic stem cells (hESCs) remains unknown. Here, we find that the loss of BACH1 in hESCs ...attenuates the expression of VSMC marker genes, whereas overexpression of BACH1 after mesoderm induction increases the expression of VSMC markers during in vitro hESC-VSMC differentiation. Mechanistically, BACH1 binds directly to coactivator-associated arginine methyltransferase 1 (CARM1) during in vitro hESC-VSMC differentiation, and this interaction is mediated by the BACH1 bZIP domain. BACH1 recruits CARM1 to VSMC marker gene promoters and promotes VSMC marker expression by increasing H3R17me2 modification, thus facilitating in vitro VSMC differentiation from hESCs after the mesoderm induction. The increased expression of VSMC marker genes by BACH1 overexpression is partially abolished by inhibition of CARM1 or the H3R17me2 inhibitor TBBD in hESC-derived cells. These findings highlight the critical role of BACH1 in hESC differentiation into VSMCs by CARM1-mediated methylation of H3R17.
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•Deletion of BACH1 attenuates VSMC differentiation from hESCs•BACH1 promotes VSMC marker expression by CARM1-mediated H3R17me2•BACH1 interacts with CARM1
He et al. find that transcription factor BACH1 acts as a positive regulator for in vitro vascular smooth muscle cell (VSMC) differentiation from human embryonic stem cells (hESCs) after mesoderm induction. They show that arginine methyltransferase CARM1-mediated histone 3 arginine 17 methylation is essential for BACH1-mediated VSMC differentiation.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
