scholarly journals The miR-203a Regulatory Network Affects the Proliferation of Chronic Myeloid Leukemia K562 Cells

2021 ◽  
Vol 9 ◽  
Author(s):  
Jinhua He ◽  
Zeping Han ◽  
Ziyi An ◽  
Yumin Li ◽  
Xingyi Xie ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Transcription Initiation ◽  
Promoter Region ◽  
Target Genes ◽  
Mononuclear Cells ◽  
K562 Cells ◽  
Luciferase Reporter ◽  
Upstream Promoter ◽  
Upstream Promoter Region

To study the molecular mechanism by which miR-203a affects the development of CML, bioinformatics software was used to predict the upstream transcription factors and downstream target genes of miR-203a. A 5’-rapid amplification of cDNA ends assay was performed to detect gene transcription initiation sites. A chromatin immunoprecipitation assay was used to verify the binding of transcription factors and promoter regions. A double luciferase reporter gene vector was constructed to demonstrate the regulatory effect of miR-203a on target genes. Real-time PCR and western blotting were used to detect the relative expression levels of genes and proteins, respectively. The results showed that there was a binding site for the transcription factor EGR1 in the upstream promoter region of miR-203a. WT1, BMI1, and XIAP were identified as target genes regulated by miR-203a. EGR1 and miR-203a were downregulated in human peripheral blood mononuclear cells and the CML K562 cell line, while WT1, BMI1, and XIAP were upregulated. The transcription initiation site of miR-203a was identified in the upstream promoter region (G nucleotide at −339 bp), and the transcription factor EGR1 could bind to the promoter region (at −268 bp) of miR-203a and increase its expression. Over expression of miR-203a inhibited the proliferation of K562 cells. A rescue assay showed that overexpression of WT1, BMI1, and XIAP offset the antitumor effect of miR-203a. Conclusion, EGR1 positively regulated the expression of miR-203a, thus relieving the inhibition of miR-203a on the translation of its target genes (WT1, BMI1, and XIAP) and affecting the proliferation of K562 cells.

Independent 5' and 3'-end determination of multiple dihydrofolate reductase transcripts

1987 ◽  
Vol 7 (10) ◽  
pp. 3732-3739
Author(s):  
J Y Yen ◽  
R E Kellems
Keyword(s):  
Dihydrofolate Reductase ◽  
Relative Abundance ◽  
Transcription Initiation ◽  
Promoter Region ◽  
Overlapping Genes ◽  
Cytoplasmic Rna ◽  
Upstream Promoter ◽  
Upstream Promoter Region ◽  
Polyadenylation Sites

Multiple dihydrofolate reductase (dhfr) mRNAs, differing substantially in abundance, are produced as a result of the utilization of multiple transcription initiation sites and multiple polyadenylation sites. We have shown that dhfr mRNAs initiating from an upstream promoter region utilize the same collection of six polyadenylation sites and generate multiple dhfr mRNAs at the same relative abundance as do the mRNAs initiating from the major transcription promoter region. These results indicate that the 5' and 3' ends of dhfr mRNAs are independently determined. We show that the relative abundance of steady-state dhfr mRNAs was the same in nuclear and cytoplasmic RNA fractions. This finding makes it unlikely that differences in mRNA stability account for differences in the relative abundance of the multiple dhfr mRNAs in the cytoplasm. Our analysis of the dhfr promoter region revealed the existence of stable cytoplasmic polyadenylated transcripts complementary to the first 300 nucleotides of the dhfr transcripts initiating from the upstream promoter region. Therefore, the dhfr locus hosts two divergent and partially overlapping genes which share the same promoter region.

scholarly journals PhoP-Responsive Expression of the Salmonella enterica Serovar Typhimurium slyA Gene

2003 ◽  
Vol 185 (12) ◽  
pp. 3508-3514 ◽  
Author(s):  
Valia A. Norte ◽  
Melanie R. Stapleton ◽  
Jeffrey Green
Keyword(s):  
Transcription Factors ◽  
Salmonella Enterica ◽  
Promoter Region ◽  
External Signal ◽  
Dependent Manner ◽  
Factors Analysis ◽  
Upstream Promoter ◽  
Serovar Typhimurium ◽  
Transcription Regulators ◽  
Upstream Promoter Region

ABSTRACT The SlyA protein of Salmonella enterica serovar Typhimurium is a member of the MarR family of transcription regulators and is required for virulence and survival in professional macrophages. Isolated SlyA protein was able to bind a specific DNA target without posttranslational modification. This suggested that SlyA might not be activated by directly sensing an external signal but rather that the intracellular concentration of SlyA is enhanced in appropriate environments through the action of other transcription factors. Analysis of slyA transcription reveals the presence of a promoter region located upstream of the previously recognized SlyA repressed promoter. The newly identified upstream promoter region did not respond to SlyA but was activated by Mg(II) starvation in a PhoP-dependent manner. We present here evidence for a direct link between two transcription factors (PhoP and SlyA) crucial for Salmonella virulence.

Abstract 267: Opposing Functions of Two Splice Variants of the Human Transcription Factor Grainyhead-like 3 in Endothelial Cells And in vivo

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Joachim Altschmied ◽  
Nicole Büchner ◽  
Sascha Jakob ◽  
Sabrina Farrokh ◽  
Christine Goy ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Target Genes ◽  
Splice Variants ◽  
Luciferase Reporter ◽  
Dependent Manner ◽  
Active Transcription ◽  
Human Transcription Factor

Grainyhead-like 3 (GRHL3) is a member of the evolutionary conserved Grainyhead family of transcription factors. In humans, three isoforms are derived from differential first exon usage and alternative splicing, which differ only in their N-terminus. Isoform 2, the only variant also present in mouse, is required for endothelial cell (EC) migration and protects against apoptosis. The functions of the human specific isoforms 1 and 3, which are derived from an alternatively spliced pre-mRNA, have not yet been investigated, although all three isoforms are expressed in EC. Therefore, we have assessed their effects on EC migration and apoptosis. Overexpression of the two proteins had opposite effects on EC migration, with isoform 1 acting pro-migratory. This protein also protected EC against apoptosis in an eNOS-dependent manner, whereas isoform 3 had no effect. These opposing outcomes with respect to apoptosis EC were corroborated by isoform-specific knockdowns. With reporter assays using a GRHL3-specific luciferase reporter we demonstrated that both are active transcription factors. Microarray analyses revealed that they induce divergent target gene sets in EC. Two validated targets, Akt2 and Mxi1, which are upregulated by isoform1, are regulators of Akt1-, and thus eNOS-phosphorylation and apoptosis, which could explain the effects of this protein on these processes. In vivo, overexpression of isoform 3 in zebrafish embryos resulted in increased lethality and severe deformations, while isoform 1 had no deleterious effect. In conclusion, our data demonstrate that the splice variant derived isoforms 1 and 3 of the human transcription factor GRHL3 induce opposing effects in primary human endothelial cells and in a whole animal model, most likely through the induction of different target genes.

Gfi1b Association to Human Hematological Abnormalities.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3748-3748
Author(s):  
Ana Villegas ◽  
Fernando A. Gonzalez ◽  
Eduardo Anguita
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Acute Leukemia ◽  
Point Mutations ◽  
K562 Cells ◽  
Vector System ◽  
Luciferase Reporter ◽  
Human Pathology ◽  
Hematological Abnormalities

Abstract Lineage specific transcription factors play essential roles in regulation of hematopoietic development. Transcription factor abnormalities have been frequently described in acute leukemia, mostly through cytogenetic changes. Nevertheless, point mutations can be easily missed. Recently, mutations in the erythroid and megakaryocyte specific transcription factor GATA1 have been discovered in patients with dyserythropoietic anemia and acute megakaryoblastic leukemia (AML-M7) with Down syndrome. Besides GATA-1, located on the X-chromosome, point mutations have been described in biallelic genes. This is the case of AML1 (RUNX1). PU1 and C/EBPalpha also represent examples of transcription factors in which point mutations are found in leukemia. A new zinc finger transcription factor involved in erythropoiesis is Gfi1b. Gfi1b was recently identified by sequence homology with oncogene Gfi1. Gfi1b knockout has demonstrated that this gene is essential for development of both erythroid and megakaryocytic lineages, and in its absence no enucleated erythrocytes are produced. Several Gfi1b DNA and protein targets (GATA1, Gfi1, AML1, p21WAF1, IL-6 Socs1 and Socs2) have been described that might be involved in malignancy. These findings indicate that Gfi1b is at the centre of hematopoiesis and may be a good candidate gene to be involved in hematological abnormalities. We have searched for Gfi1b point mutations in 122 patients with acute leukemia of all FAB types at diagnosis or relapse and 9 cases of congenital dyserythropoietic anemia. We have amplified Gfi1b promoter, coding and non-coding exons (Nucleic Acids Res2004;32:3935–46, MN 004188) by high fidelity PCR and screen for point mutations through dHPLC (Wave, Transgenomic) followed by sequencing of the cases with abnormal pattern. SNIPs in the promoter and exons were further confirmed in at least another PCR, cloned in pGEM-T easy vector system (Promega) and sequenced. Alleles with promoter SNIPs were cloned in pGL3-Enhancer vector (Promega), and transiently cotransfected with pEGFP-C2 (Clontech) to K562 cells. Luciferase activity was determined with Dual-Luciferase Reporter Assay (Promega). We found two promoter SNIPs in sequences conserved from chicken to human, one of them affecting a GATA-1 site, reducing promoter in vitro activity by 60 and 50% respectively. We also discovered a congenital exonic SNIP causing a mammalian conserved serine change to leucine. We excluded these to be frequent polymorphisms by dHPLC analysis of 96 blood donors. Although we cannot at present establish a clear relation between the former SNIPS and leukemia, we will discuss the presence of other milder hematological abnormalities. So far this is the first report of Gfi1b mutations that can be related to human pathology.

AML1-ETO Represses Multiple Transcription Factor Induced CTSG Activation by Reducing H3 Acetylation

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 3750-3750
Author(s):  
Yun Tan ◽  
Wen Jin ◽  
Kang Wu ◽  
Kankan Wang
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Target Genes ◽  
Conflicts Of Interest ◽  
Critical Role ◽  
Negative Regulator ◽  
Cathepsin G ◽  
Luciferase Reporter ◽  
Aberrant Expression ◽  
H3 Acetylation

Abstract Acute myeloid leukemia (AML) is often accompanied with the aberrant expression of transcription factors. In t(8;21) AML, the AML1-ETO fusion protein executes its critical role in leukemogenesis through the interference with hematopoietic transcription factors (TFs) including AML1, C/EBPα, PU.1 and c-Myb. These transcription factors cooperate to modulate hematopoiesis by regulating their differentiation-related target genes. In our previous work, we have identified that AML1-ETO suppresses the AML1-dependent transactivation of the gene encoding the neutrophil granule protease, cathepsin G (CTSG). However, the detailed mechanisms of AML1-ETO mediated transrepression, especially coordinated regulation of hematopoietic transcription factors, have not been characterized yet. To investigate the regulatory pattern of CTSG by hematopoietic specific transcription factors, we constructed a luciferase reporter containing the CTSG promoter and co-transfect it with AML1, c-Myb, C/EBPα or PU.1 to 293T cells. The results of luciferase assays showed that these TFs individually activated the CTSG promoter, and synergistic transactivation occurred between AML1 and c-Myb, C/EBPα and PU.1, and PU.1 and c-Myb on the CTSG promoter. Furthermore, AML1/ETO effectively suppressed the transcription factor-dependent transactivation and synergistic transactivation of the CTSG promoter. Chromatin immunoprecipitation assays further demonstrated that AML1-ETO coexisted with these TFs on the CTSG promoter in AML1/ETO-positive Kasumi-1 cell line, indicating AML1-ETO was tethered to the chromatin bound by these TFs. The data suggested that AML1-ETO might act as a negative regulator by interfering the normal function of hematopoietic TFs instead of competing for their binding. In addition, to reveal the underlying mechanism of AML1/ETO-mediated transcription repression at the epigenetic level, we examined the epigenetic status of the CTSG promoter in AML1-ETO negative and positive cells, and found the level of histone H3 Lys9 acetylation on the CTSG promoter was obviously lower in AML1-ETO positive cells than that in AML1-ETO negative cells. The data suggested that AML1-ETO might repress the gene transcription by changing the H3 acetylation status of its target gene. Collectively, our findings demonstrate that AML1-ETO represses the transactivation of the CTSG promoter mediated by multiple hematopoietic transcription factors through a decrease of H3 acetylation. Disclosures: No relevant conflicts of interest to declare.

Isolation and Characterization of Human ADAMTS13 Gene Promoter Region - Control of ADAMTS13 Gene Expression by Hepatic Transcription Factors and Inflammatory Cytokines.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1603-1603 ◽  
Author(s):  
Xingwu Zheng ◽  
Masami Niiya ◽  
X. Long Zheng ◽  
Eleanor S. Pollak
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Inflammatory Cytokines ◽  
Binding Sites ◽  
Transcription Initiation ◽  
Promoter Region ◽  
Promoter Activity ◽  
Initiation Site ◽  
Luciferase Reporter ◽  
Tnf Alpha

Abstract ADAMTS13 (A Disintegrin And Metalloprotease with ThromboSpondin type 1 repeats-13) controls von Willebrand factor multimer sizes by cleaving the Tyr1605-Met1606 bond in the central A2 domain. Deficiency of plasma ADAMTS13 activity can result in a lethal syndrome, thrombotic thrombocytopenic purpura (TTP). ADAMTS13 is primarily synthesized in hepatic stellate cells (HSCs), endothelial cells and megakaryocytes. We determined the transcription initiation site, the core region for promoter activity, the putative transcription factor binding sites as well as the influence of inflammatory cytokines on ADAMTS13 promoter activity. To explore the transcriptional control of ADAMTS13 gene expression, we constructed reporter genes containing 991 base pairs (bp) of the ADAMTS13 5′ untranslated (UT) region. We showed by deletion mutagenesis and luciferase reporter expression that the proximal-most 197 bp region was required for maximal luciferase activity in transfected cells in the human hepatic stellate cell line (LX-2) and in the human hepatocyte-like cell line (HepG2); the major transcription initiation site determined by 5′ - RACE was found at 77 bp upstream from the translation start site (ATG). However, the minimal sequences that were required for the promoter activity varied depending on the cells, with required sequences of approximately 147 and 127 bp in LX-2 and HepG2 cells, respectively. The proximal ADAMTS13 promoter region is evolutionally conserved between humans, mice and rats. This region is rich in GC content (72%) and contains putative binding sites for the transcription factors heat shock factor-2 (HSF2), FOXa2 [also named hepatocyte nuclear factor 3beta (HNF-3b)] and AP-1. A footprint assay demonstrated that the region between −116 and −126, containing the putative FOXa2 binding site, was largely protected by Dnase I digestion. The luciferase reporter activity was suppressed in cells transfected with the plasmid containing the proximal 314 bp human 5′ UT ADAMTS13 sequence in parallel with the inflammatory cytokines found to be elevated in patients with TTP: IL-4, TNF-alpha and INF-gamma. These inflammatory cytokines inhibited the Adamts13 mRNA and protein expression in rat primary HSCs in culture in a dose dependent manner. Approximately 70%, 71% and 80% of Adamts13 mRNA (by real time RT-PCR) and 77%, 78% and 92% of Adamts13 proteolytic activity (by FRETS-VWF73) were suppressed at 48 hours by IL-4 (10 ng/ml), TNF-alpha (10 ng/ml) and INF-gamma (100 ng/ml), respectively. We conclude that under physiological conditions ADAMTS13 synthesis may be strictly maintained at relatively low levels by binding transcription factors, whereas under pathological conditions inflammatory cytokines, released due to systemic inflammation, may further suppress ADAMTS13 gene expression, which may result in thrombotic complications. However, the mechanism regarding how the inflammatory cytokines negatively regulate ADAMTS13 (or Adamts13) synthesis remains to be determined.

scholarly journals Transcription of the Drosophila melanogaster 5S RNA gene requires an upstream promoter and four intragenic sequence elements.

1988 ◽  
Vol 8 (3) ◽  
pp. 1266-1274 ◽  
Author(s):  
S J Sharp ◽  
A D Garcia
Keyword(s):  
Transcription Factor ◽  
Drosophila Melanogaster ◽  
Transcription Factors ◽  
Transcription Initiation ◽  
Start Site ◽  
Transcription Start ◽  
5S Rna ◽  
Upstream Promoter ◽  
5S Dna ◽  
Control Regions

Linker-scanning (LS) mutations were constructed spanning the length of the Drosophila melanogaster 5S RNA gene. In vitro transcription analysis of the LS 5S DNAs revealed five transcription control regions. One control region essential for transcription initiation was identified in the 5'-flanking sequence. The major sequence determinants of this upstream promoter region were located between coordinates -39 and -26 (-30 region), but important sequences extended to the transcription start site at position 1. Since mutations in the upstream promoter did not alter the ability of 5S DNA to sequester transcription factors into a stable transcription complex, it appears that this control region involved the interaction of RNA polymerase III. Active 5S DNA transcription additionally required the four intragenic control regions (ICRs) located between coordinates 3 and 18 (ICR I), 37 and 44 (ICR II), 48 and 61 (ICR III), and 78 and 98 (ICR IV). LS mutations in each ICR decreased the ability of 5S DNA to sequester transcription factors. ICR III, ICR IV, and the spacer sequence between were similar in sequence and position to the determinant elements of the multipartite ICR of Xenopus 5S DNA. The importance of ICR III and ICR IV in transcription initiation and in sequestering transcription factors suggests the presence of an activity in D. melanogaster similar to transcription factor TFIIIA of Xenopus laevis and HeLa cells. Transcription initiation of Drosophila 5S DNA was not eliminated by LS mutations in the spacer region even though these mutations reduced the ability of the TFIIIA-like activity to bind. The previously unidentified control regions ICR I and ICR II appear to be important for the interaction of a transcription factor activity, or multiple-factor activities, distinct from the TFIIIA-like activity. The interaction of this activity with ICR I directed the selection of the transcription start site.

scholarly journals Independent 5' and 3'-end determination of multiple dihydrofolate reductase transcripts.

1987 ◽  
Vol 7 (10) ◽  
pp. 3732-3739 ◽  
Author(s):  
J Y Yen ◽  
R E Kellems
Keyword(s):  
Dihydrofolate Reductase ◽  
Relative Abundance ◽  
Transcription Initiation ◽  
Promoter Region ◽  
Overlapping Genes ◽  
Cytoplasmic Rna ◽  
Upstream Promoter ◽  
Upstream Promoter Region ◽  
Polyadenylation Sites

Multiple dihydrofolate reductase (dhfr) mRNAs, differing substantially in abundance, are produced as a result of the utilization of multiple transcription initiation sites and multiple polyadenylation sites. We have shown that dhfr mRNAs initiating from an upstream promoter region utilize the same collection of six polyadenylation sites and generate multiple dhfr mRNAs at the same relative abundance as do the mRNAs initiating from the major transcription promoter region. These results indicate that the 5' and 3' ends of dhfr mRNAs are independently determined. We show that the relative abundance of steady-state dhfr mRNAs was the same in nuclear and cytoplasmic RNA fractions. This finding makes it unlikely that differences in mRNA stability account for differences in the relative abundance of the multiple dhfr mRNAs in the cytoplasm. Our analysis of the dhfr promoter region revealed the existence of stable cytoplasmic polyadenylated transcripts complementary to the first 300 nucleotides of the dhfr transcripts initiating from the upstream promoter region. Therefore, the dhfr locus hosts two divergent and partially overlapping genes which share the same promoter region.

Transcription of the Drosophila melanogaster 5S RNA gene requires an upstream promoter and four intragenic sequence elements

1988 ◽  
Vol 8 (3) ◽  
pp. 1266-1274
Author(s):  
S J Sharp ◽  
A D Garcia
Keyword(s):  
Transcription Factor ◽  
Drosophila Melanogaster ◽  
Transcription Factors ◽  
Transcription Initiation ◽  
Start Site ◽  
Transcription Start ◽  
5S Rna ◽  
Upstream Promoter ◽  
5S Dna ◽  
Control Regions

Linker-scanning (LS) mutations were constructed spanning the length of the Drosophila melanogaster 5S RNA gene. In vitro transcription analysis of the LS 5S DNAs revealed five transcription control regions. One control region essential for transcription initiation was identified in the 5'-flanking sequence. The major sequence determinants of this upstream promoter region were located between coordinates -39 and -26 (-30 region), but important sequences extended to the transcription start site at position 1. Since mutations in the upstream promoter did not alter the ability of 5S DNA to sequester transcription factors into a stable transcription complex, it appears that this control region involved the interaction of RNA polymerase III. Active 5S DNA transcription additionally required the four intragenic control regions (ICRs) located between coordinates 3 and 18 (ICR I), 37 and 44 (ICR II), 48 and 61 (ICR III), and 78 and 98 (ICR IV). LS mutations in each ICR decreased the ability of 5S DNA to sequester transcription factors. ICR III, ICR IV, and the spacer sequence between were similar in sequence and position to the determinant elements of the multipartite ICR of Xenopus 5S DNA. The importance of ICR III and ICR IV in transcription initiation and in sequestering transcription factors suggests the presence of an activity in D. melanogaster similar to transcription factor TFIIIA of Xenopus laevis and HeLa cells. Transcription initiation of Drosophila 5S DNA was not eliminated by LS mutations in the spacer region even though these mutations reduced the ability of the TFIIIA-like activity to bind. The previously unidentified control regions ICR I and ICR II appear to be important for the interaction of a transcription factor activity, or multiple-factor activities, distinct from the TFIIIA-like activity. The interaction of this activity with ICR I directed the selection of the transcription start site.

scholarly journals Regulatory Network Analysis in Estradiol-Treated Human Endothelial Cells

2021 ◽  
Vol 22 (15) ◽  
pp. 8193
Author(s):  
Daniel Pérez-Cremades ◽  
Ana B. Paes ◽  
Xavier Vidal-Gómez ◽  
Ana Mompeón ◽  
Carlos Hermenegildo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Regulatory Network ◽  
Mirna Target ◽  
Target Genes ◽  
Functional Characterization ◽  
Human Endothelial Cells ◽  
Mrna Targets ◽  
Canonical Pathways

Background/Aims: Estrogen has been reported to have beneficial effects on vascular biology through direct actions on endothelium. Together with transcription factors, miRNAs are the major drivers of gene expression and signaling networks. The objective of this study was to identify a comprehensive regulatory network (miRNA-transcription factor-downstream genes) that controls the transcriptomic changes observed in endothelial cells exposed to estradiol. Methods: miRNA/mRNA interactions were assembled using our previous microarray data of human umbilical vein endothelial cells (HUVEC) treated with 17β-estradiol (E2) (1 nmol/L, 24 h). miRNA–mRNA pairings and their associated canonical pathways were determined using Ingenuity Pathway Analysis software. Transcription factors were identified among the miRNA-regulated genes. Transcription factor downstream target genes were predicted by consensus transcription factor binding sites in the promoter region of E2-regulated genes by using JASPAR and TRANSFAC tools in Enrichr software. Results: miRNA–target pairings were filtered by using differentially expressed miRNAs and mRNAs characterized by a regulatory relationship according to miRNA target prediction databases. The analysis identified 588 miRNA–target interactions between 102 miRNAs and 588 targets. Specifically, 63 upregulated miRNAs interacted with 295 downregulated targets, while 39 downregulated miRNAs were paired with 293 upregulated mRNA targets. Functional characterization of miRNA/mRNA association analysis highlighted hypoxia signaling, integrin, ephrin receptor signaling and regulation of actin-based motility by Rho among the canonical pathways regulated by E2 in HUVEC. Transcription factors and downstream genes analysis revealed eight networks, including those mediated by JUN and REPIN1, which are associated with cadherin binding and cell adhesion molecule binding pathways. Conclusion: This study identifies regulatory networks obtained by integrative microarray analysis and provides additional insights into the way estradiol could regulate endothelial function in human endothelial cells.

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