PARP7i Clinical Candidate RBN-2397 Exerts Antiviral Activity by Modulating Interferon-β Associated Innate Immune Response in Macrophages.

Polyadenosine diphosphate-ribose polymerase 7 (PARP7) acts as a suppressor of the type I interferon (IFN) signaling pathway via suppressing TANK-binding protein 1 (TBK1). Research study indicates that inhibition of PARP7 could potentially regulate tumor immunity. However, the effect of PARP7 inhibition on innate antiviral immunity in macrophages as well as the underlying mechanism have not been demonstrated else well.

Baicalin promotes antibacterial defenses by modulating mitochondrial function.

Natural flavonoids, such as baicalin, have been extensively studied for their role in bacterial infection. However, the underlying mechanisms remain poorly understood. We demonstrated that baicalin coordinates mitochondrial function and dynamics to promote antibacterial response.

Elf4 regulates lysosomal biogenesis and the mTOR pathway to promote clearance of Staphylococcus aureus in macrophages.

Staphylococcus aureus is a major cause of infectious disease. Macrophages can directly destroy most of the invading bacteria through the phagolysosomal pathway. E74-like factor 4 (Elf4) is one of the important transcription factors that controls diverse pathogens, but the role of Elf4 in macrophage-mediated S.

Ambient PM chronic exposure leads to cognitive decline in mice: From pulmonary to neuronal inflammation.

Fine particulate matter 2.5 (PM), one of the main components of air pollutants, seriously threatens human health. Possible neuronal dysfunction induced by PM has received extensive attention.

IL-1R alleviates cognitive deficits through microglial M2 polarization in AD mice.

The neuroinflammatory response is considered a crucial event in the pathology of Alzheimer's disease (AD). Neurotoxic amyloid β (Aβ) oligomers activate neuronal glial cells, leading to the elevated generation of a large variety of inflammatory factors. Therefore, the regulation of interleukin-1 receptor (IL-1R) activity is believed to be a potential target for AD therapy.

MiR-221 activates the NF-κB pathway by targeting A20.

MicroRNAs play an important role in regulating the inflammatory response, and are critically involved in the development of inflammatory disorders, including those affecting the lungs. While the microRNA miR-221 is involved in embryonic lung branching morphogenesis and epithelial cell development, its importance in lung inflammation has not been previously explored. In our current study, expression of miR-221 was selectively decreased by exposure to lipopolysaccharides (LPS) both in vitro and in vivo.

Hepatitis B Virus X Protein Sensitizes TRAIL-Induced Hepatocyte Apoptosis by Inhibiting the E3 Ubiquitin Ligase A20.

Hepatitis B virus (HBV) infection causes hepatocyte death and liver damage, which may eventually lead to cirrhosis and liver cancer. Hepatitis B virus X protein (HBx) is a key antigen that is critically involved in HBV-associated liver diseases. However, the molecular basis for its pathogenesis, particularly in liver damage, has not been well defined.

MiR-127 modulates macrophage polarization and promotes lung inflammation and injury by activating the JNK pathway.

A polarized macrophage response is presumed to have a pivotal role in a variety of immunological pathophysiology. However, the molecular mechanism underlying macrophage functional shaping remains largely unknown. In this study, we reveal a pivotal role of miR-127 in macrophage development and thereby the pathogenesis of inflammation and lung injury.

Hepatitis B e-antigen persistency is associated with the properties of HBV-specific CD8 T cells in CHB patients.

To investigate the correlation between the HBeAg and the properties of HBV-specific CD8 T cells, as well as liver injury, serum HBV markers, liver histology, the frequency and phenotypic characteristics of CD4(+)CD25(+) Treg and HBV-pentamer(+) CD8 T cells were measured. No significant differences between the median serum ALT levels, the frequency and Foxp3 expression of CD4(+)CD25(+) Treg, and liver fibrosis were observed. Higher HBV DNA levels in HBeAg(+) patients were observed, while liver necroinflammation was more severe in HBeAg(-) patients.

APOBEC3G directly binds Hepatitis B virus core protein in cell and cell free systems.

APOBEC3G (A3G) is an intrinsic antiretroviral factor which can inhibit Hepatitis B virus (HBV) replication. This antiviral activity mainly depends on A3G incorporation into viral particles. However, the mechanisms of A3G packaging into HBV particles have not been well characterized.

Inhibition of STAT1 methylation is involved in the resistance of hepatitis B virus to Interferon alpha.

As a major therapy for hepatitis B virus (HBV) infection, Interferon alpha (IFN-alpha) triggers intracellular signal transduction including JAK-STAT pathway to produce various antiviral effector mechanisms. However, patients with chronic hepatitis B usually show low response to IFN-alpha treatment and the underlying mechanism remains unclear. In the present study, HepG2 and HepG2.

[Assembly of full-length human resistin gene in vitro and construction of its eukaryotic expression vector].

Objective: To assemble the full-length of human resistin gene in vitro by using oligonucleotides and to construct its eukaryotic expression vector.

Methods: According to the gene sequence of resistin (GenBank: AF323081), 10 oligonucleotides were designed and synthesized, followed by a touch down PCR to assemble the full-length gene. The PCR products were cloned into pSecTag2B vector and confirmed by sequencing.