Hemin regulates platelet clearance in hemolytic disease by binding to GPIbα.

Hemolysis is associated with thrombosis and vascular dysfunction, which are the pathological components of many diseases. Hemolytic products, including hemoglobin and hemin, activate platelets (PLT). Despite its activation, the effect of hemolysis on platelet clearance remains unclear, It is critical to maintain a normal platelet count and ensure that circulating platelets are functionally viable.

CTRP4/interleukin-6 receptor signaling ameliorates autoimmune encephalomyelitis by suppressing Th17 cell differentiation.

C1q/TNF-related protein 4 (CTRP4) is generally thought to be released extracellularly and plays a critical role in energy metabolism and protecting against sepsis. However, its physiological functions in autoimmune diseases have not been thoroughly explored. In this study, we demonstrate that Th17 cell-associated experimental autoimmune encephalomyelitis was greatly exacerbated in Ctrp4-/- mice compared with WT mice due to increased Th17 cell infiltration.

Laponite Lights Calcium Flickers by Reprogramming Lysosomes to Steer DC Migration for An Effective Antiviral CD8 T-Cell Response.

Immunotherapy using dendritic cell (DC)-based vaccination is an established approach for treating cancer and infectious diseases; however, its efficacy is limited. Therefore, targeting the restricted migratory capacity of the DCs may enhance their therapeutic efficacy. In this study, the effect of laponite (Lap) on DCs, which can be internalized into lysosomes and induce cytoskeletal reorganization via the lysosomal reprogramming-calcium flicker axis, is evaluated, and it is found that Lap dramatically improves the in vivo homing ability of these DCs to lymphoid tissues.

A possible strategy for generating polymer chains with an entanglement-free structure.

We propose a possible strategy that may experimentally generate long polymeric chains with an entanglement-free structure. The basic idea is designing the conditions to restrict polymer chains from growing along the surface with an obviously concave curvature. This strategy is proved to effectively reduce the chance of forming both inter- and intra-molecular entanglements, which is quite similar to the self-avoiding random walking of chains on a two dimensional plane.

FAM96A suppresses epithelial-mesenchymal transition and tumor metastasis by inhibiting TGFβ1 signals.

Metastasis is the main cause of death in 90% of patients with tumors, and epithelial-mesenchymal transition (EMT) plays a key role in this process. Family with sequence similarity 96 member A (FAM96A) is an evolutionarily conserved protein related to cytosolic iron assembly. However, no research has been conducted on its role in tumor metastasis.

Establishment of a Novel Mouse Hepatocellular Carcinoma Model for Dynamic Monitoring of Tumor Development by Bioluminescence Imaging.

In this study, a novel mouse model of hepatocellular carcinoma (HCC) was established by simultaneously knocking out Pten and p53 suppressor genes and overexpressing c-Met and △90-β-catenin proto-oncogenes in the livers of mice hydrodynamic injection (HDI). The mutations were introduced using the CRISPR/Cas9 and Sleeping Beauty transposon systems. In this way, a primary liver cancer model was established within six weeks.

PTPIP51 inhibits non-small-cell lung cancer by promoting PTEN-mediated EGFR degradation.

Protein tyrosine phosphatase interacting protein 51 (PTPIP51) interacts with two non-receptor tyrosine phosphatases and induces apoptosis. In the present study, we showed that PTPIP51 is downregulated in non-small cell lung cancer (NSCLC), and its elevated expression correlates with improved outcomes. PTPIP51 overexpression in NSCLC cells significantly inhibits downstream epidermal growth factor receptor (EGFR) signaling in PI3K/Akt, RAS/RAF/ERK, and JAK/STAT3 pathways.

CTRP4 acts as an anti-inflammatory factor in macrophages and protects against endotoxic shock.

Despite the availability of antibiotics, current therapies to treat sepsis are still ineffective and many clinical trials aimed at neutralizing specific inflammatory cytokines have failed, suggesting the urgent need for new treatments. Using two models of LPS-induced endotoxemia and cecal ligation and puncture (CLP)-induced sepsis, we investigated the effects of C1q/TNF-related protein 4(CTRP4) on septic lethality and sepsis-induced inflammation. The effects of CTRP4 on survival, inflammation, organ damage, and bacterial clearance were assessed.

FAM96A Protects Mice From Dextran Sulfate Sodium (DSS)-Induced Colitis by Preventing Microbial Dysbiosis.

Family with sequence similarity 96 member A (FAM96A) is an evolutionarily conserved intracellular protein that is involved in the maturation of the Fe/S protein, iron regulatory protein 1 (IRP1), and the mitochondria-related apoptosis of gastrointestinal stromal tumor cells. In this study, we used a mouse model of chemically induced colitis to investigate the physiological role of FAM96A in intestinal homeostasis and inflammation. At baseline, colons from mice exhibited microbial dysbiosis, dysregulated epithelial cell turnover, an increased number of goblet cells, and disordered tight junctions with functional deficits affecting intestinal permeability.

In vitro study of FUZ as a novel potential therapeutic target in non-small-cell lung cancer.

FUZ is regarded as a planar cell polarity effector that controls multiple cellular processes during vertebrate development. However, the role of FUZ in tumor biology remains poorly studied. Our purpose of this study is to discover the physiological effects and mechanism of FUZ in non-small-cell lung cancer (NSCLC) in vitro.

TMEM74 promotes tumor cell survival by inducing autophagy via interactions with ATG16L1 and ATG9A.

Autophagy is a highly inducible system of intracellular degradation that occurs in lysosomes or vacuoles. Transmembrane 74 (TMEM74) has been shown to induce autophagy. However, the mechanism by which TMEM74 stimulates autophagy and the impacts of TMEM74-induced autophagy on tumor cell survival remain unclear.

SZRD1 is a Novel Protein that Functions as a Potential Tumor Suppressor in Cervical Cancer.

is a novel gene screened out by high-throughput platform, and so far there exists no systematic function reports. The purpose of our study is to discover the function and mechanism of this novel human gene. Bioinformatics analysis indicates that SZRD1 is a highly conserved intracellular protein.

Autophagy regulatory molecule, TMEM74, interacts with BIK and inhibits BIK-induced apoptosis.

TMEM74 (Transmembrane protein 74), a lysosome transmembrane protein, induces cell autophagy. Knockdown of TMEM74 abolished EBSS-induced autophagy. BIK, belonging to BOP (BH3-only protein) protein family, has been reported to induce cell apoptosis.