Erratum: -methyladenosine-induced ERRγ triggers chemoresistance of cancer cells through upregulation of ABCB1 and metabolic reprogramming: Erratum.

[This corrects the article DOI: 10.7150/thno.40144.

Identification of broad neutralizing antibodies against Omicron subvariants from COVID-19 convalescents and vaccine recipients.

• BF.7 and BQ.1, escaped most neutralizing antibodies isolated from the recovered COVID-19 individuals and vaccine recipients.

HDAC8 promotes the dissemination of breast cancer cells via AKT/GSK-3β/Snail signals.

The mechanistic action of histone deacetylase 8 (HDAC8) in cancer motility, including epithelial-mesenchymal transition (EMT), remains largely undefined. We found that the expression of HDAC8 was upregulated in breast cancer (BC) cells and tissues as compared to the controls. Further, BC tissues had the highest values of HDAC8 expression among 31 kinds of cancers.

N-methyladenosine regulates glycolysis of cancer cells through PDK4.

Studies on biological functions of N-methyladenosine (mA) modification in mRNA have sprung up in recent years. We find mA can positively regulate the glycolysis of cancer cells. Specifically, mA-sequencing and functional studies confirm that pyruvate dehydrogenase kinase 4 (PDK4) is involved in mA regulated glycolysis and ATP generation.

Targeted mRNA demethylation using an engineered dCas13b-ALKBH5 fusion protein.

Studies on biological functions of N6-methyladenosine (m6A) modification in mRNA have drawn significant attention in recent years. Here we describe the construction and characterization of a CRISPR-Cas13b-based tool for targeted demethylation of specific mRNA. A fusion protein, named dm6ACRISPR, was created by linking a catalytically inactive Type VI-B Cas13 enzyme from Prevotella sp.

-methyladenosine-induced ERRγ triggers chemoresistance of cancer cells through upregulation of ABCB1 and metabolic reprogramming.

: Drug resistance severely reduces treatment efficiency of chemotherapy and leads to poor prognosis. However, regulatory factors of chemoresistant cancer cells are largely unknown. : The expression of estrogen receptor related receptors (ERRs) in chemoresistant cancer cells are checked.

N6-Methyladenosine Regulates the Expression and Secretion of TGFβ1 to Affect the Epithelial-Mesenchymal Transition of Cancer Cells.

N6-methyladenosine (mA) is the most abundant modification on eukaryotic mRNA, which regulates all steps of the mRNA life cycle. An increasing number of studies have shown that mA methylation plays essential roles in tumor development. However, the relationship between mA and the progression of cancers remains to be explored.

N6-methyladenosine induced miR-143-3p promotes the brain metastasis of lung cancer via regulation of VASH1.

Background: Brain metastasis (BM) is one of the principal causes of mortality for lung cancer patients. While the molecular events that govern BM of lung cancer remain frustrating cloudy.

Methods: The miRNA expression profiles are checked in the paired human BM and primary lung cancer tissues.

Neuron activity-induced Wnt signaling up-regulates expression of brain-derived neurotrophic factor in the pain neural circuit.

Brain-derived neurotrophic factor (BDNF) is a master regulator of synaptic plasticity in various neural circuits of the mammalian central nervous system. Neuron activity-induced BDNF gene expression is regulated through the Ca/CREB pathway, but other regulatory factors may also be involved in controlling BDNF levels. We report here that Wnt/β-catenin signaling plays a key role in controlling neuron activity-regulated BDNF expression.

A role of the mammalian target of rapamycin (mTOR) in glutamate-induced down-regulation of tuberous sclerosis complex proteins 2 (TSC2).

Mammalian target of rapamycin (mTOR) signaling plays a critical role in the regulation of activity-dependent protein synthesis in neurons. It is well established that the GTPase-activating protein tuberous sclerosis complex proteins (2TSC2) is an upstream inhibitor of mTOR. In this study, we show that glutamate stimulation down-regulates TSC2 protein in cortical cultures via NMDA receptor (NMDAR) activation.