gopubmed logo
 
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Cell cycle exit and neuronal differentiation 1

BM88, Cend1, BM88 antigen
The protein encoded by this gene is a neuron-specific protein. The similar protein in pig enhances neuroblastoma cell differentiation in vitro and may be involved in neuronal differentiation in vivo. Multiple pseudogenes have been reported for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, ACID, V1a, PCNA, TUBE
Papers on BM88
CEND1 and NEUROGENIN2 Reprogram Mouse Astrocytes and Embryonic Fibroblasts to Induced Neural Precursors and Differentiated Neurons.
New
Thomaidou et al., Athens, Greece. In Stem Cell Reports, Oct 2015
Here we explored the effect of CEND1 and NEUROG2 on reprogramming of mouse cortical astrocytes and embryonic fibroblasts.
Downregulation of BM88 after optic nerve injury.
Ball et al., Hamilton, Canada. In Invest Ophthalmol Vis Sci, 2014
PURPOSE: BM88 is a cell-cycle exit and neuronal differentiation protein that has been used as a marker of surviving retinal ganglion cells (RGCs) after optic nerve injury.
Neural stem cell transplantation in an animal model of traumatic brain injury.
Thomaidou, Athens, Greece. In Methods Mol Biol, 2013
Along these lines, in this review we describe a protocol which involves transplantation of NPCs, genetically engineered to overexpress the neurogenic molecule Cend1 and have thus the potency to differentiate with higher frequency towards the neuronal lineage in a rodent model of stab wound cortical injury.
Marked methylation changes in intestinal genes during the perinatal period of preterm neonates.
Sangild et al., Shenzhen, China. In Bmc Genomics, 2013
In the 4 d-old formula-fed preterm pigs, four genes associated with intestinal metabolism (CYP2W1, GPR146, TOP1MT, CEND1) showed significant hyper-methylation in their promoter CGIs, and thus, down-regulated transcription.
Loss of Ahi1 affects early development by impairing BM88/Cend1-mediated neuronal differentiation.
Li et al., Changsha, China. In J Neurosci, 2013
Mass spectrometry analysis of cytosolic Ahi1 immunoprecipitates reveals that Ahi1 also binds Cend1 (cell cycle exit and neuronal differentiation protein 1)/BM88, a neuronal protein that mediates neuronal differentiation and is highly expressed in postnatal mouse brain.
Functional Interactions between BM88/Cend1, Ran-binding protein M and Dyrk1B kinase affect cyclin D1 levels and cell cycle progression/exit in mouse neuroblastoma cells.
Gaitanou et al., Athens, Greece. In Plos One, 2012
BM88/Cend1 is a neuronal-lineage specific modulator with a pivotal role in coordination of cell cycle exit and differentiation of neuronal precursors.
Neural stem cells transplanted in a mouse model of Parkinson's disease differentiate to neuronal phenotypes and reduce rotational deficit.
Kouvelas et al., Pátrai, Greece. In Cns Neurol Disord Drug Targets, 2012
Over-expression of the cell cycle exit and neuronal differentiation protein Cend1 in NPCs enhances the generation of GABAergic, but not dopaminergic, neuronal phenotypes after grafting in the lesioned striatum.
[Culture and induced multilineage differentiation of mesenchymal stem cells derived from human nasal mucosa].
Zhang et al., Zhenjiang, China. In Lin Chuang Er Bi Yan Hou Ke Za Zhi, 2012
The induced cells expressed neural markers NF-200 and BM88 strongly.
Proteomics, ultrastructure, and physiology of hippocampal synapses in a fragile X syndrome mouse model reveal presynaptic phenotype.
Li et al., Amsterdam, Netherlands. In J Biol Chem, 2011
A group of proteins that are known to be involved in cell differentiation and neurite outgrowth was regulated; they included Basp1 and Gap43, known PKC substrates, and Cend1.
Impaired cerebellar development and deficits in motor coordination in mice lacking the neuronal protein BM88/Cend1.
GeneRIF
Matsas et al., Athens, Greece. In Mol Cell Neurosci, 2010
Our results suggest that Cend1 is required for normal cerebellar development.
C38, equivalent to BM88, is developmentally expressed in maturing retinal neurons and enhances neuronal maturation.
Yamada et al., Ōsaka, Japan. In J Neurochem, 2010
Sequence analysis of C38 cDNA revealed that C38 is equivalent to rat BM88, which has been reported to induce cell-cycle arrest and neuronal differentiation in Neuro2a cells.
Transplantation of embryonic neural stem/precursor cells overexpressing BM88/Cend1 enhances the generation of neuronal cells in the injured mouse cortex.
GeneRIF
Matsas et al., Athens, Greece. In Stem Cells, 2010
Transplantation of BM88/Cend1-overexpressing neural progenitor cells exerts beneficial effects on tissue regeneration by enhancing the number of generated neurons and restricting the formation of astroglial scar, in a mouse model of cortical brain injury.
BM88/Cend1 regulates stimuli-induced intracellular calcium mobilization.
Matsas et al., Athens, Greece. In Neuropharmacology, 2009
We have previously demonstrated that BM88 is a neuronal lineage-specific regulator of cell cycle exit and differentiation; we now report a link between BM88 and calcium signaling.
BM88/Cend1 expression levels are critical for proliferation and differentiation of subventricular zone-derived neural precursor cells.
GeneRIF
Thomaidou et al., Athens, Greece. In Stem Cells, 2008
BM88/Cend1 participates in cell cycle control and neuronal differentiation mechanisms during neonatal SVZ neurogenesis and becomes crucial for the transition from neuroblasts to mature neurons when reaching high levels
Coordination of cell cycle exit and differentiation of neuronal progenitors.
Review
Matsas et al., Athens, Greece. In Cell Cycle, 2008
BM88/Cend1 is a neuronal protein associated in vivo with terminal neuron-generating divisions, marking the exit of proliferative cells from the cell cycle.
BM88/CEND1 coordinates cell cycle exit and differentiation of neuronal precursors.
GeneRIF
Matsas et al., Athens, Greece. In Proc Natl Acad Sci U S A, 2007
Results implicate BM88 in the synchronization of cell cycle exit and differentiation of neuronal precursors in the developing nervous system.
Expression pattern of BM88 in the developing nervous system of the chick and mouse embryo.
GeneRIF
Matsas et al., Athens, Greece. In Gene Expr Patterns, 2007
BM88 is widely expressed in the embryonic CNS and PNS, in both nestin-positive neuroepithelial cells and post-mitotic betaIII-tubulin positive neurons.
share on facebooktweetadd +1mail to friends