Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1242/dev.122317 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Adult Neurogenesis Is Altered by Circadian Phase Shifts and the Duper Mutation in Female Syrian Hamsters.
eNeuro
March 2023
Program in Neuroscience and Behavior, University of Massachusetts, Amherst, Massachusetts 01003
Cell birth and survival in the adult hippocampus are regulated by a circadian clock. Rotating shift work and jet lag disrupt circadian rhythms and aggravate disease. Internal misalignment, a state in which abnormal phase relationships prevail between and within organs, is proposed to account for adverse effects of circadian disruption.
View Article and Find Full Text PDFDCLK1 promotes colorectal cancer stemness and aggressiveness via the XRCC5/COX2 axis.
Theranostics
August 2022
School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, 61005, Republic of Korea.
Doublecortin-like kinase 1 (DCLK1) is a serine/threonine kinase that selectively marks cancer stem-like cells (CSCs) and promotes malignant progression in colorectal cancer (CRC). However, the exact molecular mechanism by which DCLK1 drives the aggressive phenotype of cancer cells is incompletely determined. Here, we performed comprehensive genomics and proteomics analyses to identify binding proteins of DCLK1 and discovered X-ray repair cross-complementing 5 (XRCC5).
View Article and Find Full Text PDFInhibition of KDM1A activity restores adult neurogenesis and improves hippocampal memory in a mouse model of Kabuki syndrome.
Mol Ther Methods Clin Dev
March 2021
McKusick-Nathans Department of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Kabuki syndrome (KS) is a rare cause of intellectual disability primarily caused by loss-of-function mutations in lysine-specific methyltransferase 2D (), which normally adds methyl marks to lysine 4 on histone 3. Previous studies have shown that a mouse model of KS ( ) demonstrates disruption of adult neurogenesis and hippocampal memory. Proof-of-principle studies have shown postnatal rescue of neurological dysfunction following treatments that promote chromatin opening; however, these strategies are non-specific and do not directly address the primary defect of histone methylation.
View Article and Find Full Text PDFDoublecortin-Like Is Implicated in Adult Hippocampal Neurogenesis and in Motivational Aspects to Escape from an Aversive Environment in Male Mice.
eNeuro
June 2021
Department of Cell and Chemical Biology
Doublecortin (DCX)-like (DCL) is a microtubule (MT)-associated protein (MAP) that is highly homologous to DCX and is crucially involved in embryonic neurogenesis. Here, we have investigated the role of DCL in adult hippocampal neurogenesis by generating transgenic mice producing inducible shRNA molecules that specifically target DCL but no other splice variants produced by the DCLK gene. DCL knock-down (DCL-KD) resulted in a significant increase in the number of proliferating BrdU+ cells in the subgranular zone (SGZ) 1 d after BrdU administration.
View Article and Find Full Text PDFDoublecortin undergo nucleocytoplasmic transport via the RanGTPase signaling to promote glioma progression.
Cell Commun Signal
February 2020
Department of Neurobiology and Anatomy, Key Laboratory of Neurobiology, Xuzhou Medical University, 209, Tongshan Road, Xuzhou, 221004, China.
Background: Nuclear translocation of several oncogenic proteins have previously been reported, but neither the translocation of doublecortin (DCX) nor the mechanism involved has been studied. DCX is a neuronal microtubule-associated protein (MAP) that is crucial for adult neurogenesis and neuronal migration and has been associated with poor prognosis in gliomas.
Methods: We probed DCX expression in different grades of glioma tissues and conventional cells via western blotting.
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!