An animal model recapitulates human hepatic diseases associated with mutations.

Heterozygotic mutations are responsible for various congenital diseases in the heart, pancreas, liver, and other organs in humans. However, there is lack of an animal that can comprehensively model these diseases since GATA6 is essential for early embryogenesis. Here, we report the establishment of a knockout zebrafish which recapitulates most of the symptoms in patients with mutations, including cardiac outflow tract defects, pancreatic hypoplasia/agenesis, gallbladder agenesis, and various liver diseases.

Parental ADHD knowledge and medical visit status of school-aged children in Shanghai.

Introduction: The diagnosis and care of children and adolescents with neurodevelopmental disorders presents a public health crisis in China. Attention deficit hyperactivity disorder (ADHD) is one of the most frequent conditions. Many Chinese children and adolescents with ADHD are underdiagnosed and undertreated.

Ufmylation on UFBP1 alleviates non-alcoholic fatty liver disease by modulating hepatic endoplasmic reticulum stress.

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease characterized by lipid accumulation and endoplasmic reticulum (ER) stress, while effective therapies targeting the specific characteristics of NAFLD are limited. Ufmylation is a newly found post-translational modification process that involves the attachment of the Ubiquitin-fold modifier 1 (UFM1) protein to its substrates via ufmylation modification system. Ufmylation regulates ER stress via modifying UFM1 binding protein 1 (UFBP1), suggesting a potential role for ufmylation in NAFLD pathogenesis.

TRAIP serves as a potential prognostic biomarker and correlates with immune infiltrates in lung adenocarcinoma.

Background: Lung adenocarcinoma (LUAD) is one of the major types of lung cancer with high morbidity and mortality. The TRAF-interacting protein (TRAIP) is a ring-type E3 ubiquitin ligase which has been recently identified to play pivotal roles in various cancers. However, the expression and function of TRAIP in LUAD remain elusive.

P4HB UFMylation regulates mitochondrial function and oxidative stress.

UFMylation is a ubiquitin-like modification which attaches the ubiquitin-fold modifier 1 to target proteins. To date, only a few UFMylation targets have been identified. In the current study, we demonstrated that P4HB is a new target protein for UFMylation and it can be UFMylated at three lysine residues in the form of mono-UFMylation.

miR-185-5p Regulates Inflammation and Phagocytosis through CDC42/JNK Pathway in Macrophages.

Macrophage activation is an essential component of systemic chronic inflammation and chronic inflammatory diseases. Emerging evidence implicates miR-185-5p in chronic inflammation diseases. However, the regulatory role of miR-185-5p in macrophage pro-inflammatory activation has not been studied previously.

Corrigendum: Functioning of Long Noncoding RNAs Expressed in Macrophage in the Development of Atherosclerosis.

[This corrects the article DOI: 10.3389/fphar.2020.

The Ribosome Biogenesis Factor Ltv1 Is Essential for Digestive Organ Development and Definitive Hematopoiesis in Zebrafish.

Ribosome biogenesis is a fundamental activity in cells. Ribosomal dysfunction underlies a category of diseases called ribosomopathies in humans. The symptomatic characteristics of ribosomopathies often include abnormalities in craniofacial skeletons, digestive organs, and hematopoiesis.

lncRNA PANTR1 Upregulates BCL2A1 Expression to Promote Tumorigenesis and Warburg Effect of Hepatocellular Carcinoma through Restraining miR-587.

Hepatocellular carcinoma (HCC) is one of the most common subtypes of malignant liver tumors, characterized by high morbidity and mortality. Due to its poor diagnosis strategy and inefficient clinical intervention, HCC has brought terrible life experiences for patients worldwide. Finding novel curative agents for HCC is urgently needed.

Functioning of Long Noncoding RNAs Expressed in Macrophage in the Development of Atherosclerosis.

Chronic inflammation is part of the pathological process during atherosclerosis (AS). Due to the abundance of monocytes/macrophages within the arterial plaque, monocytes/macrophages have become a critical cellular target in AS studies. In recent decades, a number of long noncoding RNAs (lncRNAs) have been found to exert regulatory roles on the macrophage metabolism and macrophage plasticity, consequently promoting or suppressing atherosclerotic inflammation.

Hsa_circ_0000345 regulates the cellular development of ASMCs in response to oxygenized low-density lipoprotein.

The interaction between circRNAs and atherosclerosis has been extensively studied. However, more novel circRNAs need to be explored to help establish a perfect regulatory network. In the present research, hsa_circ_0000345 was demonstrated to regulate cellular development of oxygenized low-density lipoprotein (ox-LDL)-treated aortic smooth muscle cells (ASMCs), which was closely related to the occurrence and progress of atherosclerosis.

Circular RNA has_circ_0003204 inhibits oxLDL-induced vascular endothelial cell proliferation and angiogenesis.

Circular RNAs (circRNAs) are widely expressed in eukaryotic cells and play a key role in atherosclerosis. The aim of this study is to explore the relationship between hsa_circ_0003204 and atherosclerosis. Here, hsa_circ_0003204 was aberrantly overexpressed in the ox-LDL-induced human umbilical vein endothelial cells (HUVECs).

Analysis of mutants from a genetic screening reveals the control of intestine and liver development by many common genes in zebrafish.

Both the intestine and liver develop from the endoderm, yet little is known how these two digestive organs share and differ in their developmental programs, at the molecular level. A classical forward genetic screen, with no gene bias, is an effective way to address this question by examining the defects of the intestine and liver in obtained mutants to assess mutated genes responsible for the development of either organ or both. We report here such a screen in zebrafish.