Novel gene function and regulation in neocortex expansion.

Curr Opin Cell Biol

Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstr. 108, D-01307 Dresden, Germany. Electronic address:

Published: December 2017

The expansion of the neocortex during human evolution is due to changes in our genome that result in increased and prolonged proliferation of neural stem and progenitor cells during neocortex development. Three principal types of such genomic changes can be distinguished, first, novel gene regulation in human, second, novel function in human of genes existing in both human and non-human species, and third, novel, human-specific genes. The latter comprise both, increases in the copy number of genes existing also in non-human species, and the emergence of genes giving rise to unique, human-specific gene products. Examples of all these types of changes in the human genome have been identified, with ARHGAP11B constituting a paradigmatic example of a unique, human-specific protein.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.ceb.2017.11.008DOI Listing

Publication Analysis

Top Keywords

novel gene
8
genes existing
8
non-human species
8
unique human-specific
8
human
5
novel
4
gene function
4
function regulation
4
regulation neocortex
4
neocortex expansion
4

Similar Publications

Lysine demethylases (KDMs) catalyze the oxidative removal of the methyl group from histones using earth-abundant iron and the metabolite 2-oxoglutarate (2OG). KDMs have emerged as master regulators of eukaryotic gene expression and are novel drug targets; small-molecule inhibitors of KDMs are in the clinical pipeline for the treatment of human cancer. Yet, mechanistic insights into the functional heterogeneity of human KDMs are limited, necessitating the development of chemical probes for precision targeting.

View Article and Find Full Text PDF

Based on the notion that hypomorphic germline genetic variants are linked to autoimmune diseases, we reasoned that novel targets for cancer immunotherapy might be identified through germline variants associated with greater T-cell infiltration into tumors. Here, we report that while investigating germline polymorphisms associated with a tumor immune gene signature, we identified PKCδ as a candidate. Genetic deletion of PKCδ in mice resulted in improved endogenous antitumor immunity and increased efficacy of anti-PD-L1.

View Article and Find Full Text PDF

CircZMYM2 Alleviates TGF-β1-Induced Proliferation, Migration and Activation of Fibroblasts via Targeting miR-199b-5p/KLF13 Axis.

Appl Biochem Biotechnol

January 2025

Department of Respiratory and Critical Care Medicine, Tianjin Medical University General Hospital Affiliated to Tianjin Medical University, No.154 Heping Road to Anshan, Tianjin City, 300052, People's Republic of China.

Dysregulated circular RNAs (circRNAs) has been revealed to be involved in pulmonary fibrosis progression. Herein, this study focused on exploring the function and mechanism of circRNA Zinc Finger MYM-Type Containing 2 (circZMYM2) on idiopathic pulmonary fibrosis (IPF) using transforming growth factor (TGF)-β1-stimulated fibroblasts. Human fibroblast cell lines IMR-90 and HFL1 were stimulated with TGF-β1 to mimic fibrosis condition in vitro.

View Article and Find Full Text PDF

Novel Protective Role for Gut Microbiota-derived Metabolite PAGln in Doxorubicin-induced Cardiotoxicity.

Cardiovasc Drugs Ther

January 2025

Department of Pharmacy, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China.

Purpose: Doxorubicin (Dox) is a classic anthracycline chemotherapy drug with cause cumulative and dose-dependent cardiotoxicity. This study aimed to investigate the potential role and molecular mechanism of phenylacetylglutamine (PAGln), a novel gut microbiota metabolite, in Dox-induced cardiotoxicity (DIC).

Methods: DIC models were established in vivo and in vitro, and a series of experiments were performed to verify the cardioprotective effect of PAGln.

View Article and Find Full Text PDF

The multifaceted roles of aldolase A in cancer: glycolysis, cytoskeleton, translation and beyond.

Hum Cell

January 2025

Institute of Translational Medicine, Medical College, Yangzhou University, No. 136 Jiangyangzhonglu, Yangzhou, 225009, Jiangsu, China.

Cancer, a complicated disease characterized by aberrant cellular metabolism, has emerged as a formidable global health challenge. Since the discovery of abnormal aldolase A (ALDOA) expression in liver cancer for the first time, its overexpression has been identified in numerous cancers, including colorectal cancer (CRC), breast cancer (BC), cervical adenocarcinoma (CAC), non-small cell lung cancer (NSCLC), gastric cancer (GC), hepatocellular carcinoma (HCC), pancreatic cancer adenocarcinoma (PDAC), and clear cell renal cell carcinoma (ccRCC). Moreover, ALDOA overexpression promotes cancer cell proliferation, invasion, migration, and drug resistance, and is closely related to poor prognosis of patients with cancer.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!