ArticleMolecular and cellular biology2001
Identification of TFII-I as the endoplasmic reticulum stress response element binding factor ERSF: its autoregulation by stress and interaction with ATF6.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed.
- Molecular characterization of the ER stress-inducible factor CRELD2.Cell biochemistry and biophysics · 2024Article
- Loss of GTF2I promotes neuronal apoptosis and synaptic reduction in human cellular models of neurodevelopment.Cell reports · 2024Article
- Intricate subcellular journey of nanoparticles to the enigmatic domains of endoplasmic reticulum.Drug delivery · 2023Review
- Identification of a peptide ligand for human ALDH3A1 through peptide phage display: Prediction and characterization of protein interaction sites and inhibition of ALDH3A1 enzymatic activity.Frontiers in molecular biosciences · 2023Article
- Pdia4 regulates β-cell pathogenesis in diabetes: molecular mechanism and targeted therapy.EMBO molecular medicine · 2021Article
- Ultrabright plasmonic fluor nanolabel-enabled detection of a urinary ER stress biomarker in autosomal dominant tubulointerstitial kidney disease.American journal of physiology. Renal physiology · 2021Article
- Die Wechselwirkung mit ribosomalen Proteinen begleitet die Stressinduktion des Wirkstoffkandidaten BOLD-100/KP1339 im endoplasmatischen Retikulum.Angewandte Chemie (Weinheim an der Bergstrasse, Germany) · 2021Article
- Interaction with Ribosomal Proteins Accompanies Stress Induction of the Anticancer Metallodrug BOLD-100/KP1339 in the Endoplasmic Reticulum.Angewandte Chemie (International ed. in English) · 2021Article
- Dermatan Sulfate Is a Potential Regulator of IgHFrontiers in immunology · 2021Article
- Regulation of RNA Polymerase II Transcription Initiation and Elongation by Transcription Factor TFII-I.Frontiers in molecular biosciences · 2021Review
- Article
- The contribution of GTF2I haploinsufficiency to Williams syndrome.Molecular and cellular probes · 2018Review
- Lipid environment induces ER stress, TXNIP expression and inflammation in immune cells of individuals with type 2 diabetes.Diabetologia · 2018Article
- Functional interrelationship between TFII-I and E2F transcription factors at specific cell cycle gene loci.Journal of cellular biochemistry · 2018Article
- Identification of additional loci associated with antibody response to Mycobacterium avium ssp. Paratuberculosis in cattle by GSEA-SNP analysis.Mammalian genome : official journal of the International Mammalian Genome Society · 2017Article
- Protein disulfide isomerase a4 acts as a novel regulator of cancer growth through the procaspase pathway.Oncogene · 2017Article
- GRP78 at the Centre of the Stage in Cancer and Neuroprotection.Frontiers in neuroscience · 2017Review
- Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases.Acta pharmacologica Sinica · 2016Review
- Identification of novel regulatory NFAT and TFII-I binding elements in the calbindin-D28k promoter in response to serum deprivation.Biochemical and biophysical research communications · 2015Article
- The Human Adenovirus Type 5 L4 Promoter Is Negatively Regulated by TFII-I and L4-33K.Journal of virology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
When mammalian cells are subjected to stress targeted to the endoplasmic reticulum (ER), such as depletion of the ER Ca(2+) store, the transcription of a family of glucose-regulated protein (GRP) genes encoding ER chaperones is induced. The GRP promoters contain multiple copies of the ER stress response element (ERSE), consisting of a unique tripartite structure, CCAAT(N(9))CCACG. Within a subset of mammalian ERSEs, N(9) represents a GC-rich sequence of 9 bp that is conserved across species. A novel complex (termed ERSF) exhibits enhanced binding to the ERSE of the grp78 and ERp72 promoters using HeLa nuclear extracts prepared from ER-stressed cells. Optimal binding of ERSF to ERSE and maximal ERSE-mediated stress inducibility require the conserved GGC motif within the 9-bp region. Through chromatographic purification and subsequent microsequencing, we have identified ERSF as TFII-I. Whereas TFII-I remains predominantly nuclear in both nontreated NIH 3T3 cells and cells treated with thapsigargin (Tg), a potent inducer of the GRP stress response through depletion of the ER Ca(2+) store, the level of TFII-I transcript was elevated in Tg-stressed cells, correlating with an increase in TFII-I protein level in the nuclei of Tg-stressed cells. Purified recombinant TFII-I isoforms bind directly to the ERSEs of grp78 and ERp72 promoters. The stimulation of ERSE-mediated transcription by TFII-I requires the consensus tyrosine phosphorylation site of TFII-I and the GGC sequence motif of the ERSE. We further discovered that TFII-I is an interactive protein partner of ATF6 and that optimal stimulation of ERSE by ATF6 requires TFII-I.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.