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Many Toll-like receptors (TLRs) signal through TNF receptor-associated factor 6 (TRAF6) to activate innate immune responses. Here, we show that somatic nuclear autoantigenic sperm protein (sNASP) binds to TRAF6 to prevent TRAF6 autoubiquitination in unstimulated macrophages. Following LPS stimulation, a complex consisting of sNASP, TRAF6, IRAK4, and casein kinase 2 (CK2) is formed. CK2 phosphorylates sNASP at serine 158, allowing sNASP to dissociate from TRAF6. Free TRAF6 is then autoubiquitinated, followed by activation of downstream signaling pathways. In sNasp S158A knockin (S158A-KI) mice, LPS-treated macrophages could not phosphorylate sNASP, which remained bound to TRAF6. S158A-KI mice were more susceptible to sepsis due to a marked reduction in IL-1[beta], TNF-[alpha], and IFN-[gamma] production accompanied by an inability to clear bacteria and recruit leukocytes. Furthermore, phosphorylation-regulated release of sNASP from TRAF6 is observed following activation of TLR-1, -2, -4, -5, and -6. Thus, sNASP is a negative regulator of TLR signaling to modulate the innate immune response., Introduction The innate immune response is activated by pathogen-associated molecular patterns (PAMPs) through a family of Toll-like receptors (TLRs) (1, 2). TLR signaling can be classified into MyD88-dependent or MyD88-independent [...]

Bronchial specimens from patients with well-controlled asthma who had more intact airway epithelium were used for comparison with specimens from patients with severe asthma. Severe asthma: PP4 expression in the denuded epithelium of patients with severe asthma was very low. Loss of PP4 contributes to diesel exhaust particles-induced epithelial barrier integrity disruption and alarmins release. [Extracted from the article]

Broadband photodetectors have attracted considerable attention owing to their commercial and military applications. We report using a single Zn2GeO4 nanowire for high-performance broadband photodetectors. The Zn2GeO4 nanowires are stoichiometric, single crystal rhombohedral structure with a high concentration of intrinsic defects. The photodetector exhibits high photocurrent, high normalized gain, high detectivity, and a broad spectral response from UV to visible light. The photoresponsivities of 404 A W−1 at the UV wavelength of 325 nm, 505 A W−1 at the visible light of 405 nm, 606 A W−1 at 532 nm, and 336 A W−1 at 633 nm have been achieved. The detectivity of a device is ranging from 4.3 × 1011 to 1.2 × 1012 Jones in the spectral range from UV to visible. The broadband photoresponse characteristics of a single Zn2GeO4 nanowire photodetector are attributed to the high surface-to-volume ratio, wide bandgap, and defect-rich nature of Zn2GeO4 nanowire. In addition, the oxygen-sensitized photoconduction mechanism has been proposed. The results suggest that Zn2GeO4 nanowires are promising materials for a broadband flexible photodetector under harsh environments. [ABSTRACT FROM AUTHOR]

WRKY transcription factors play a key role in the tolerance of biotic and abiotic stresses across various crop species, but the function of some WRKY genes, particularly in tomato, remains unexplored. Here, we characterize the roles of a previously unstudied WRKY gene, SlWRKY8, in the resistance to pathogen infection and the tolerance to drought and salt stresses. Expression of SlWRKY8 was up‐regulated upon Pseudomonas syringae pv. tomato DC3000 (Pst. DC3000), abiotic stresses such as drought, salt and cold, as well as ABA and SA treatments. The SlWRKY8 protein was localized to the nucleus with no transcription activation in yeast, but it could activate W‐box‐dependent transcription in plants. The overexpression of SlWRKY8 in tomato conferred a greater resistance to the pathogen Pst. DC3000 and resulted in the increased transcription levels of two pathogen‐related genes SlPR1a1 and SlPR7. Moreover, transgenic plants displayed the alleviated wilting or chlorosis phenotype under drought and salt stresses, with higher levels of stress‐induced osmotic substances like proline and higher transcript levels of the stress‐responsive genes SlAREB, SlDREB2A and SlRD29. Stomatal aperature was smaller under drought stress in transgenic plants, maintaining higher water content in leaves compared with wild‐type plants. The oxidative pressure, indicated by the concentration of hydrogen peroxide (H2O2) and malondialdehyde (MDA), was also reduced in transgenic plants, where we also observed higher levels of antioxidant enzyme activities under stress. Overall, our results suggest that SlWRKY8 functions as a positive regulator in plant immunity against pathogen infection as well as in plant responses to drought and salt stresses. [ABSTRACT FROM AUTHOR]

The board plays a central role in monitoring the management on behalf of shareholders, yet the efficacy of board monitoring is difficult to determine. This study proposes using board attendance as a proxy measure of board supervisory quality and investigates the factors influencing board attendance, as well as their impact on firms’ performance, by conducting a second-order regression analysis. The results show that board attendance decreases with multiple directorships, meeting frequency, and board size, indicating that busier directors and a more complex board combine to lower meeting attendance. The director shareholding rate and proportion of independent directors increase with board attendance, implying the convergence of interest among directors and companies and that strong external monitoring prompts higher board attendance. Finally, we find that higher board attendance enhances higher firm accounting performance, verifying that firms could view the attendance rate as an indication of the quality of the board supervision of these corporate monitors. [ABSTRACT FROM PUBLISHER]

SUMMARY Mobile Worldwide Interoperability for Microwave Access networks usually provide flexible sleep-mode operations that allow mobile stations to conserve energy during sleep or active mode. For example, the IEEE 802.16e/m standard presents three power-saving classes that can be associated with different types of network connections to decrease the power consumption of mobile stations. However, previous studies failed to fully use the sleep-mode features to save energy of a mobile station while simultaneously maintaining unicast and multicast/broadcast connections. This study proposes an energy-efficient packet scheduling algorithm for both multicast and broadcast services that does not violate the QoS requirements of real-time connections. The proposed activity aggregation selection mechanism approach can minimize total power consumption of mobile stations in one cell and simultaneously satisfy the QoS of real-time connections. This method improves energy efficiency for IEEE 802.16e/m and the activity aggregation selection mechanism approach can optimize sleeping mode features to save the energy of mobile stations with overlapping connection packets The simulations in this study verified the proposed approach.Copyright © 2012 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

SUMMARY Because the bandwidth usage of wireless transmission is limited, one of the major research topics in this field is to improve system throughput by supporting multiple users with limited bandwidth resources. Although there are several studies on cross-layer designs for improving system throughput, previous research on quality-of-service guarantee and fairness are relatively rare. This study proposes a cross-layer subcarrier permutation (CLSP) mechanism that uses cross-layer strategies to select suboptimal subcarriers. Service flows simulations in the IEEE 802.16e system indicate that CLSP achieved a lower delay time and a long-term fairness among multiple users. Experimental results further show that the throughput of CLSP is 28 percent higher than that of the partial usage of subchannels model using the orthogonal frequency division multiple access technique. Copyright © 2011 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Many Toll-like receptors (TLRs) signal through TNF receptor-associated factor 6 (TRAF6) to activate innate immune responses. Here, we show that somatic nuclear autoantigenic sperm protein (sNASP) binds to TRAF6 to prevent TRAF6 autoubiquitination in unstimulated macrophages. Following LPS stimulation, a complex consisting of sNASP, TRAF6, IRAK4, and casein kinase 2 (CK2) is formed. CK2 phosphorylates sNASP at serine 158, allowing sNASP to dissociate from TRAF6. Free TRAF6 is then autoubiquitinated, followed by activation of downstream signaling pathways. In sNasp S158A knockin (S158A-KI) mice, LPS-treated macrophages could not phosphorylate sNASP, which remained bound to TRAF6. S158A-KI mice were more susceptible to sepsis due to a marked reduction in IL-1β, TNF-α, and IFN-γ production accompanied by an inability to clear bacteria and recruit leukocytes. Furthermore, phosphorylation-regulated release of sNASP from TRAF6 is observed following activation of TLR-1, -2, -4, -5, and -6. Thus, sNASP is a negative regulator of TLR signaling to modulate the innate immune response. [ABSTRACT FROM AUTHOR]

Introduction: Neurosteroids have a variety of neurological functions, such as neurite growth, neuroprotection, myelination, and neurogenesis. P450scc, encoded by CYP11A1 gene, is the cholesterol side chain cleavage enzyme that catalyzes the first and rate-limiting step in steroidogenesis. In this study, we examine the dendritic morphology in developing hippocampal neurons of Cyp11a1 null mice at P15, a critical period for synapse formation and maturation., Methods: Knockout mice were maintained until P15 with hormone administration. The Golgi-Cox method stained CA1 and CA3 pyramidal neurons in the hippocampus to reveal dendritic morphology., Results: We demonstrated that Cyp11a1 null mice usually die within 7 days after birth and thus collected brain samples at postnatal day 5 (P5) for examination. There was significant shrinkage of dendrite size and diminishment of dendritic branching in CA1 and CA3 pyramidal neurons in the hippocampus of Cyp11a1 null mice, suggesting a developmental delay. We wonder if this delay may catch up later in life. Since the age of P15 is a critical period for synapse formation and maturation, the Cyp11a1 null mice were rescued by receiving hormone administration until P15 that the dendritic morphology in the developing hippocampal neurons could be examined. The results indicated that the total dendritic length, the number of dendritic branches, as well as dendritic arborization in the CA1 and CA3 pyramidal neurons are significantly decreased in P15 knockout mice when compared to the wild type. The spine densities were also significantly decreased. In addition, the Western blot analysis revealed decreased PSD-95 expression levels in the knockout mice compared to the wild type at P15., Conclusion: These results suggested that Cyp11a1 deficiency impairs the dendritic structures in the developing hippocampal pyramidal neurons., (© 2024 The Author(s). Published by S. Karger AG, Basel.)

SUMO protease SENP1 is elevated in multiple carcinomas including prostate cancer (PCa). SENP1 exhibits carcinogenic properties; it promotes androgen receptor-dependent and -independent cell proliferation, stabilizes HIF1α, increases VEGF, and supports angiogenesis. However, mice expressing an androgen-responsive promoter driven SENP1-transgene (SENP1-Tg) develop high-grade prostatic intraepithelial neoplasia, but not carcinoma. We now show that tumor suppressive PTEN signaling is induced in SENP1-Tg to enhance prostate epithelial cell apoptosis. SENP1 blocks SUMO1-dependent ubiquitylation and degradation of PTEN. In the absence of SENP1, SUMO1-modified PTEN is sequestered in the cytosol, where binding to ubiquitin-E3 ligase WWP2 occurs. Concurrently, WWP2 is also SUMOylated, which potentiates its interaction with PTEN. Thus, SENP1 directs ubiquitin-E3-substrate association to control PTEN stability. PTEN serves as a barrier for SENP1-mediated prostate carcinogenesis as SENP1-Tg mice develop invasive carcinomas only after PTEN reduction. Hence, SENP1 modulates multiple facets of carcinogenesis and may serve as a target specifically for aggressive PTEN-deficient PCa.