Last update 01 Nov 2024

MIER1

Last update 01 Nov 2024

Basic Info

Synonyms

Early response 1, Er1, hMI-ER1

+ [5]

Introduction

Transcriptional repressor regulating the expression of a number of genes including SP1 target genes. Probably functions through recruitment of HDAC1 a histone deacetylase involved in chromatin silencing.

Drugs associated with MIER1

CN118184735

Patent Mining

Target

MIER1

Mechanism-

Active Org.

Nanjing Medical University

Originator Org.

Nanjing Medical University

Active Indication

Gastrointestinal Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MIER1

100 Translational Medicine associated with MIER1

0 Patents (Medical) associated with MIER1

177

Literatures (Medical) associated with MIER1

01 Nov 2024·Neuroscience

Bulk and single-cell RNA-seq analyses reveal canonical RNA editing associated with microglia homeostasis and its role in sepsis-associated encephalopathy

Article

Author: Wang, Li-Ping ; Zhu, Lin ; Gao, Di ; Wu, Jun-Fan ; Jin, Yun-Yun ; Liu, Yan-Shan ; Pan, Xu-Bin ; Li, Yu-Ning ; Feng, Yan-Meng ; Chen, Jian-Huan ; Wei, Zhi-Yuan ; Shi, Jia ; Tang, Xiao-Dan

Previous studies have demonstrated the roles of both microglia homeostasis and RNA editing in sepsis-associated encephalopathy (SAE), yet their relationship remains to be elucidated. In this study, we analyzed bulk and single-cell RNA-seq (scRNA) datasets containing 107 brain tissue and microglia samples from mice with microglial depletion and repopulation to explore canonical RNA editing associated with microglia homeostasis and evaluate its role in SAE. Analysis of mouse brain RNA-Seq revealed hallmarks of microglial repopulation, including peak expressions of Apobec1 and Apobec3 at Day 5 of repopulation and dramatically altered B2m RNA editing. Significant time-dependent changes in brain RNA editing during microglial depletion and repopulation were primarily observed in synapse-related genes, such as Tbc1d24 and Slc1a2. ScRNA-Seq revealed heterogeneous RNA editing among microglia subpopulations and their distinct changes associated with microglia homeostasis. Moreover, repopulated microglia from lipopolysaccharide (LPS)-induced sepsis mice exhibited intensified up-regulation of Apobec1 and Apobec3, with distinct RNA editing responses to LPS, mainly involved in immune-related pathways. The hippocampus from sepsis mice induced by peritoneal contamination and infection showed upregulated Apobec1 and Apobec3 expression, and altered RNA editing in immune-related genes, such as B2m and Mier1, and nervous-related lncRNA Meg3 and Snhg11, both of which were repressed by microglial depletion. Furthermore, the expression of complement-related genes, such as C4b and Cd47, was substantially correlated with RNA editing activity in microglia homeostasis and SAE. Our study demonstrates canonical RNA editing associated with microglia homeostasis and provides new insights into its potential role in SAE.

01 Oct 2024·Plant Disease

Three Novel er1 Alleles and Their Functional Markers for Breeding Resistance to Powdery Mildew (Erysiphe pisi) in Pea

Article

Author: Deng, Dong ; Zhan, Junliang ; Wu, Wenqi ; Sun, Suli ; Duan, Canxing ; Wang, Danhua ; Zhu, Zhendong

Powdery mildew caused by Erysiphe pisi DC is a global notorious disease on peas. Deploying resistance pea cultivars is the most efficient and environmentally friendly method for disease control. This study focuses on revealing the resistance genes in three pea germplasms and developing their functional markers for resistance breeding. The identification of resistance genes involved genetic mapping and the sequencing of the pea mildew resistance locus O homolog PsMLO1 gene. To confirm the heredity of three resistant germplasms, they were crossed with susceptible cultivars to generate F1, F2, and F2:3 populations. The F1 generation exhibited susceptibility to E. pisi, whereas the segregation patterns in subsequent generations adhered to the 3:1 (susceptible: resistant) and 1:2:1 (susceptible homozygotes: heterozygotes: resistant homozygotes) ratios, indicating that powdery mildew resistance was governed by a single recessive gene in each germplasm. Analysis of er1-linked markers and genetic mapping suggested that the resistance genes could be er1 alleles in these germplasms. The multiple clone sequencing results of the three homologous PsMLO1 genes showed they were novel er1 alleles, named er1-15, er1-16, and er1-17. The er1-15 and er1-16 were caused by 1-bp deletion at position 335 (A) and 429 (T) in exon 3, respectively, whereas er1-17 was caused by a 1-bp insertion at position 248 in exon 3, causing a frame-shift mutation and premature termination of PsMLO1 protein translation. Their respective functional markers, kompetitive allele-specific PCR (KASP)-er1-15, KASP-er1-16, and KASP-er1-17, were successfully developed and validated in respective mapping populations and pea germplasms. These results provide valuable tools for pea breeding resistance to E. pisi.

01 Sep 2024·Metabolism Open

Acute liver steatosis signals the chromatin for regeneration via MIER1

Author: Xiong, Jie ; Liu, Junli ; Chen, Suzhen

During liver regeneration, especially after a hepatectomy, hepatocytes experience significant lipid accumulation. These transiently accumulated lipids are generally believed to provide substrates for energy supply or membrane biomaterials for newly generated hepatocytes. Remarkably, a recent study found that acute lipid accumulation during regeneration can act as a signal for chromatin remodeling to regulate regeneration. Chen, Y.H., et al. identified MIER1 (mesoderm induction early response protein 1) as a crucial inhibitor of liver regeneration through in vivo CRISPR screening. MIER1 binds to and restrains cell cycle genes' expression. During liver regeneration, acute lipid accumulation suppresses MIER1 translation via the EIF2S pathway, resulting in transient down-regulation of MIER1 protein, which promotes cell cycle gene expression and liver regeneration. Interestingly, the researchers also found that the dynamic regulation of MIER1 was impaired in fatty and aging livers with chronic steatosis, while of knockout of MIER1 in these animals improved their regenerative capacity. In conclusion, this study provides valuable insights into the complex mechanisms underlying liver regeneration and highlights the potential therapeutic applications of targeting MIER1 for improving liver regeneration in disease states associated with impaired lipid homeostasis.

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MIER1

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