ArticleThe Journal of biological chemistry2010
Wilms tumor suppressor 1 (WT1) and early growth response 1 (EGR1) are regulators of STIM1 expression.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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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.
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Who cites it
39 citing papers in PubMed, 57 citations in OpenAlex.
- Multifaceted regulatory mechanisms of the EGR family in tumours and prospects for therapeutic applications (Review).International journal of molecular medicine · 2025Review
- The Wilms' Tumor Suppressor WT1 in Cardiomyocytes: Implications for Cardiac Homeostasis and Repair.Cells · 2024Review
- Multifaceted control of T cell differentiation by STIM1.Trends in biochemical sciences · 2023Review
- Cardiomyocyte-Specific Wt1 Is Involved in Cardiac Metabolism and Response to Damage.Journal of cardiovascular development and disease · 2023Article
- Article
- Gubernaculum and Epididymo-Testicular Descent: Review of the Literature.Acta medica Lituanic · 2022Review
- The function of the calcium channel Orai1 in osteoclast development.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Deletion of the Wilms' Tumor Suppressor Gene in the Cardiac Troponin-T Lineage Reveals Novel Functions of WT1 in Heart Development.Frontiers in cell and developmental biology · 2021Article
- Plasma Membrane Calcium ATPase Regulates Stoichiometry of CD4Frontiers in immunology · 2021Article
- Suppression of CaEMBO reports · 2020Article
- Host signaling and EGR1 transcriptional control of human cytomegalovirus replication and latency.PLoS pathogens · 2019Article
- miRNA-dependent regulation of STIM1 expression in breast cancer.Scientific reports · 2019Article
- EGR1 recruits TET1 to shape the brain methylome during development and upon neuronal activity.Nature communications · 2019Article
- EGR-mediated control of STIM expression and function.Cell calcium · 2019Review
- Zinc Finger Readers of Methylated DNA.Molecules (Basel, Switzerland) · 2018Review
- Preliminary Structure-Activity Relationship (SAR) of a Novel Series of Pyrazole SKF-96365 Analogues as Potential Store-Operated Calcium Entry (SOCE) Inhibitors.International journal of molecular sciences · 2018Article
- STIM1 (c)AMPs up melanogenesis.The EMBO journal · 2018Article
- Identification of epigenetic modulators in human breast cancer by integrated analysis of DNA methylation and RNA-Seq data.Epigenetics · 2018Article
- The transcriptional coregulatorOncotarget · 2017Article
- Stromal interaction molecule 1 haploinsufficiency causes maladaptive response to pressure overload.PloS one · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Store-operated calcium entry (SOCE) is a key evolutionarily conserved process whereby decreases in endoplasmic reticulum Ca(2+) content lead to the influx of Ca(2+) across the plasma membrane. How this process is regulated in specific tumor cell types is poorly understood. In an effort to address this concern, we obtained and tested primary Wilms tumor cells, finding no detectable SOCE in this cell type. Analysis of the expression levels of STIM1 and ORAI1 (the molecular mediators of SOC) revealed poor STIM1 expression. Analysis of the STIM1 promoter using the TESS search system (University of Pennsylvania) revealed four putative response elements to the zinc-finger proteins WT1 (Wilms tumor suppressor 1) and EGR1 (early growth response 1). Either overexpression of WT1 or knockdown of EGR1 resulted in loss of STIM1 expression and a resultant decrease in SOCE. Furthermore, examination of Egr1 knock-out animals revealed loss of STIM1 expression in multiple tissues. Finally, using chromatin immunoprecipitation, we reveal direct binding of both WT1 and EGR1 to putative response elements located within 500 bp of the transcriptional start site of STIM1. Considering that WT1 and EGR1 are well described oncogenes and tumor suppressors, these observations may reveal new mechanisms responsible for distinct Ca(2+) signals in cancer cells.
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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.