AI Article Synopsis
- EGR1 is a transcription factor that influences various biological processes like growth and apoptosis, and its dysregulation is linked to diseases such as tumors and brain disorders.
- The study identifies a new splicing isoform of the EGR1 gene, which produces a shorter protein that lacks a crucial region for its activation function.
- While this isoform can enter the nucleus, it is less effective in activating transcription compared to the standard EGR1 protein.
Article Abstract
EGR1 is a transcription factor expressed in many cell types that regulates genes involved in different biological processes including growth, proliferation, and apoptosis. Dysregulation of EGR1 expression has been associated with many pathological conditions such as tumors and brain diseases. Known molecular mechanisms underlying the control of EGR1 function include regulation of transcription, mRNA and protein stability, and post-translational modifications. Here we describe the identification of a splicing isoform for the human gene. The newly identified splicing transcript encodes a shorter protein compared to the canonical EGR1. This isoform lacks a region belonging to the N-terminal activation domain and although it is capable of entering the nucleus, it is unable to activate transcription fully relative to the canonical isoform.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6479754 | PMC |
| http://dx.doi.org/10.3390/ijms20071548 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Pennsylvania, Philadelphia, PA, USA.
Background: Tau is a neuronal microtubule associated protein whose interactions with microtubules are regulated by phosphorylation. Tau has numerous putative phosphorylation sites, but it is unclear which combinations of Tau phosphorylation co-occur in the normal state and precisely how they impact Tau function. Adding further complexity, there are six major Tau isoforms arising from alternative splicing.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
TauC3 Biologics Limited, London, United Kingdom.
Background: Tau abnormalities are a central feature of Alzheimer's disease (AD) and the defining feature of non-AD tauopathies, which include frontotemporal lobar degeneration (FTLD) due to Pick's disease (PiD) or Mapt mutations (FTLD-tau), as well as progressive supranuclear palsy (PSP), corticobasal degeneration (CBD) and others. Mapt transcripts undergo alternative splicing to produce 6 distinct isoforms. Exon 2 splicing produces 0, 1 or 2 inserts; exclusion or inclusion of exon 10 results in 3-repeat (3R) or 4-repeat (4R) forms, respectively.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
Background: Alzheimer's disease (AD) hallmarks are amyloid plaques and tau tangles. APOE and TREM2 are the strongest genetic risk factors for AD. Triggering receptor expressed on myeloid cells 2 (TREM2) is increasingly recognized to play a central role in amyloid beta clearance and microglia activation in AD.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Emory University School of Medicine, Atlanta, GA, USA.
Background: The microtubule-associated Tau gene (MAPT) undergoes alternative splicing to produce isoforms with varying combinations of microtubule-binding region (MTBR) repeats (3R, 4R). The MTBR is the predominant region that forms paired helical filaments and neurofibrillary tangles fibrils in disease. Alzheimer's disease (AD) is a mixed Tauopathy containing both 3R and 4R isoforms.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Exeter, Exeter, Devon, United Kingdom.
Background: Increasing evidence suggests that alternative splicing plays an important role in Alzheimer's disease (AD), a devastating neurodegenerative disorder involving the intracellular aggregation of hyperphosphorylated tau.
Method: We used whole transcriptome and targeted long-read cDNA sequencing to profile transcript diversity in the entorhinal cortex of wild-type (WT) and transgenic (TG) mice harbouring a mutant form of human tau.
Result: Whole transcriptome profiling showed that previously reported gene-level expression differences between WT and TG mice reflect changes in the abundance of specific transcripts.
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!