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Academic literature on the topic 'E2 gene deletion'
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Journal articles on the topic "E2 gene deletion"
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COSTEAS, Paul A., and Jeffrey M. CHINSKY. "Glucocorticoid regulation of branched-chain α-ketoacid dehydrogenase E2 subunit gene expression." Biochemical Journal 347, no. 2 (April 10, 2000): 449–57. http://dx.doi.org/10.1042/bj3470449.
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Regulation of the mammalian branched-chain α-ketoacid dehydrogenase complex (BCKAD) occurs under a variety of stressful conditions associated with changes in circulating glucocorticoids. Multiple levels of regulation in hepatocytes, including alteration of the levels of the structural subunits available for assembly (E1, α-ketoacid decarboxylase; E2, dihydrolipoamide acyltransferase; and E3, dihydrolipoamide dehydrogenase), as well as BCKAD kinase, which serves to phosphorylate the E1α subunit and inactivate complex activity, have been proposed. The direct role of glucocorticoids in regulating the expression of the murine gene encoding the major BCKAD subunit E2, upon which the other BCKAD subunits assemble, was therefore examined. Deletion analysis of the 5ʹ proximal 7.0 kb of the murine E2 promoter sequence, using E2 promoter/luciferase expression minigene plasmids introduced into the hepatic H4IIEC3 cell line, suggested a promoter proximal region responsive to glucocorticoid regulation. Linker-scanning mutagenesis combined with deletion analysis established this functional glucocorticoid-responsive unit (GRU) to be located near the murine E2 proximal promoter site at -140 to -70 bp upstream from the transcription initiation site. The presence of this region in plasmid minigenes, containing varying amounts of the murine genomic sequence 5ʹ upstream from proximal E2 promoter sequences, conferred 2-10 fold increases in luciferase reporter gene expression in H4IIEC3 cells, whether introduced by transient transfection or following co-selection for stable transfectants. The GRU region itself appeared to contain multiple interacting elements that combine to regulate overall E2 promoter activity in response to changing physiological conditions associated with varying concentrations of glucocorticoids and likely other hormonal effectors.
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Harada, Takashi, Norbert Tautz, and Heinz-Jürgen Thiel. "E2-p7 Region of the Bovine Viral Diarrhea Virus Polyprotein: Processing and Functional Studies." Journal of Virology 74, no. 20 (October 15, 2000): 9498–506. http://dx.doi.org/10.1128/jvi.74.20.9498-9506.2000.
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ABSTRACT The genes encoding pestivirus E2 and NS2-3 are separated by a sequence that encodes a small hydrophobic polypeptide with an apparent molecular mass of 6 to 7 kDa (p7). It has been shown that cleavage between E2 and p7 is incomplete, resulting in proteins E2-p7, E2, and p7. We found no precursor-product relationship between E2-p7 and E2, which indicates a stable nature of E2-p7. To study the function of the E2-p7 region of the polyprotein, mutations were introduced into an infectious cDNA of bovine viral diarrhea virus (BVDV). When cleavage between E2 and p7 was abolished, viral RNA replication occurred; however, no infectious virus could be recovered. A corresponding result was obtained with a construct encompassing a large in-frame deletion of p7. To prevent synthesis of E2-p7, a translational stop codon was introduced after the last codon of the E2 gene and an internal ribosome entry site element followed by a signal peptide coding sequence was inserted upstream of the p7 gene. Transfection of RNA transcribed from the bicistronic construct led to the release of infectious virus particles. Thus, synthesis of E2-p7 is not essential for the generation of infectious virions. Cell lines constitutively expressing BVDV p7 and/or E2 were generated for complementation studies. Transfection of BVDV RNAs with point mutations or a deletion in the E2-p7 region into the complementing cell lines led to the generation of infectious virions. According to our studies, p7 as well as E2 can be complemented in trans.
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Vyhlidal, C., X. Li, and S. Safe. "Estrogen regulation of transferrin gene expression in MCF-7 human breast cancer cells." Journal of Molecular Endocrinology 29, no. 3 (December 1, 2002): 305–17. http://dx.doi.org/10.1677/jme.0.0290305.
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Transferrin (Tf) is an iron transport protein expressed in MCF-7 human breast cancer cells. In nuclear run-on assays, 17beta-estradiol (E2) increased the rate of Tf gene expression approximately 3-fold within 1 h after treatment and reporter gene activity was also induced in MCF-7 cells transfected with a construct containing a -3600 to +39 Tf gene promoter insert. Deletion and mutation analysis identified an E2-responsive promoter region between -811 and -762, which was GC-rich (80%) and contained two nonconsensus estrogen response elements (EREs). E2-responsiveness of this region was associated with a GGACA(N)(3)TGGCC motif (-803 to -791) which bound human estrogen receptor alpha (hERalpha) in gel mobility shift assays. In Drosophila Schneider SL-2 cells, the -811 to -752 was E2-responsive after cotransfection with hERalpha expression plasmid plus E2, whereas Sp1 protein did not induce transactivation. These studies confirm that E2 induces Tf gene expression through a nonconsensus distal ERE.
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Loeken, M. R., G. Khoury, and J. Brady. "Stimulation of the adenovirus E2 promoter by simian virus 40 T antigen or E1A occurs by different mechanisms." Molecular and Cellular Biology 6, no. 6 (June 1986): 2020–26. http://dx.doi.org/10.1128/mcb.6.6.2020.
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We have examined the ability of simian virus 40 T antigen to stimulate transcription from the adenovirus E2 promoter. T antigen, produced from a cotransfected plasmid, stimulated chloramphenicol acetyltransferase enzyme and mRNA production from an E2 promoter-chloramphenicol acetyltransferase fusion plasmid (pEC113) in monkey kidney CV-1 cells. The level of stimulation of E2 transcription by simian virus 40 T antigen was equal to that observed in cotransfections of pEC113 and the adenovirus E1A gene product. Deletion mutations from the 5' end of the E2 promoter were examined for their ability to express basal, T-antigen, or E1A trans-activated promoter activity. In each case, deletion of upstream promoter sequences to -70 base pairs reduced chloramphenicol acetyltransferase expression to approximately 30% of the level observed with the intact E2 promoter. Deletion to -59 base pairs resulted in chloramphenicol acetyltransferase expression that was 3 to 5% of that observed with the intact E2 promoter. At saturating levels of the stimulatory proteins, the chloramphenicol acetyltransferase levels obtained in response to T antigen and adenovirus E1A were additive. COS-1 cells, which are derived from CV-1 cells and constitutively express simian virus 40 T antigen, do not support E2 promoter trans activation by T antigen. E1A trans activation of the E2 promoter is efficient in COS-1 cells. These results suggest that although promoter sequence requirements are similar, T antigen and E1A trans activate the E2 promoter by different mechanisms.
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Loeken, M. R., G. Khoury, and J. Brady. "Stimulation of the adenovirus E2 promoter by simian virus 40 T antigen or E1A occurs by different mechanisms." Molecular and Cellular Biology 6, no. 6 (June 1986): 2020–26. http://dx.doi.org/10.1128/mcb.6.6.2020-2026.1986.
Full textAbstract:
We have examined the ability of simian virus 40 T antigen to stimulate transcription from the adenovirus E2 promoter. T antigen, produced from a cotransfected plasmid, stimulated chloramphenicol acetyltransferase enzyme and mRNA production from an E2 promoter-chloramphenicol acetyltransferase fusion plasmid (pEC113) in monkey kidney CV-1 cells. The level of stimulation of E2 transcription by simian virus 40 T antigen was equal to that observed in cotransfections of pEC113 and the adenovirus E1A gene product. Deletion mutations from the 5' end of the E2 promoter were examined for their ability to express basal, T-antigen, or E1A trans-activated promoter activity. In each case, deletion of upstream promoter sequences to -70 base pairs reduced chloramphenicol acetyltransferase expression to approximately 30% of the level observed with the intact E2 promoter. Deletion to -59 base pairs resulted in chloramphenicol acetyltransferase expression that was 3 to 5% of that observed with the intact E2 promoter. At saturating levels of the stimulatory proteins, the chloramphenicol acetyltransferase levels obtained in response to T antigen and adenovirus E1A were additive. COS-1 cells, which are derived from CV-1 cells and constitutively express simian virus 40 T antigen, do not support E2 promoter trans activation by T antigen. E1A trans activation of the E2 promoter is efficient in COS-1 cells. These results suggest that although promoter sequence requirements are similar, T antigen and E1A trans activate the E2 promoter by different mechanisms.
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Zhao, Y.-L., W.-D. Han, Q. Li, Y.-M. Mu, X.-C. Lu, L. Yu, H.-J. Song, X. Li, J.-M. Lu, and C.-Y. Pan. "Mechanism of transcriptional regulation of LRP16 gene expression by 17-β estradiol in MCF-7 human breast cancer cells." Journal of Molecular Endocrinology 34, no. 1 (February 2005): 77–89. http://dx.doi.org/10.1677/jme.1.01628.
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LRP16 gene expression is induced by 17-βestradiol (E2) via estrogen receptor alpha (ERα) in MCF-7 human breast cancer cells. A previous study also demonstrated that ectopic expression of LRP16 gene promoted MCF-7 cell proliferation. To explore the mechanism of hormone-induced LRP16 gene expression, the LRP16 gene promoter region (−2600 to −24 bp upstream of the LRP16 gene translation starting site) was analyzed in the present study by using different 5′-truncated constructs, and a luciferase reporter. The 5′-flanking sequence of −676 to −24 bp (pGL3-S5) was found to be E2-responsive. After exchange of the fragment from −213 to −24 bp with the TK gene proximal promoter region in pGL3-S5, E2 still induced reporter gene activity in MCF-7 and HeLa cells. Sequence analysis showed that the pGL3-S6 (−676 to −214) sequence contains two motifs that may contribute to E2-induced transactivation; namely, an estrogen-responsive element (ERE) half-site/Sp1 at −246 to −227 bp and an E-box site at −225 to −219 bp. Further deletion and mutation analysis of these two motifs indicated that both the 1/2 ERE and Sp1 binding sites were required for E2 action, while E-box deletion did not affect the luciferase activity in MCF-7 and HeLa cells. The results of gel mobility shift and chromatin immunoprecipitation assays confirmed that both ERαand Sp1 were required for hormone-induced transactivation, which involved both ERαand Sp1 directly binding to DNA. Taken together, these findings suggest that ERαand Sp1 play a role in activation of the human LRP16 gene promoter.
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Panno, M. L., L. Mauro, S. Marsico, D. Bellizzi, P. Rizza, C. Morelli, M. Salerno, F. Giordano, and S. Ando’. "Evidence that the mouse insulin receptor substrate-1 belongs to the gene family on which the promoter is activated by estrogen receptor α through its interaction with Sp1." Journal of Molecular Endocrinology 36, no. 1 (February 2006): 91–105. http://dx.doi.org/10.1677/jme.1.01848.
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In the present study, the molecular mechanism underlying the up-regulatory effect of estradiol (E2) on mouse insulin receptor substrate-1 (IRS-1) promoter was investigated in CHO cells on which the same promoter had first been functionally characterized. The mouse IRS-1 promoter bears four consensus half Estrogen Responsive Elements (ERE) sequences and thirteen AP-1- and ten Sp1-binding elements. We performed molecular dissection of this promoter gene providing 3′ different deleted constructs, containing the same AP-1 rich region with a progressively increased number of ERE half sites located downstream. None of these constructs was responsive to E2, while a downstream region (nt −1420 to −160) rich in GC elements was induced by E2. However, the latter region lost its intrinsic E2 responsiveness when the whole IRS-1 promoter was mutated for deletion in all four ERE half sites. Deletion analysis of the ERE half sites demonstrated that only ERE located at the position −1500 to −1495, close to the GC-rich region, was able to maintain the induced activatory effect of E2 on the IRS-1 gene. Electrophoretic mobility shift and chromatin immunoprecipitation assays identified the region containing the half ERE/Sp1 (nt −1500 to −1477) as the one conferring E2 responsiveness to the whole promoter. This effect occurs through the functional interaction between E2/ERα and Sp1.
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Hewitt, Sylvia C., Sydney L. Lierz, Marleny Garcia, Katherine J. Hamilton, Artiom Gruzdev, Sara A. Grimm, John P. Lydon, Francesco J. Demayo, and Kenneth S. Korach. "A distal super enhancer mediates estrogen-dependent mouse uterine–specific gene transcription of Igf1 (insulin-like growth factor 1)." Journal of Biological Chemistry 294, no. 25 (May 9, 2019): 9746–59. http://dx.doi.org/10.1074/jbc.ra119.008759.
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Insulin-like growth factor 1 (IGF1) is primarily synthesized in and secreted from the liver; however, estrogen (E2), through E2 receptor α (ERα), increases uterine Igf1 mRNA levels. Previous ChIP-seq analyses of the murine uterus have revealed a potential enhancer region distal from the Igf1 transcription start site (TSS) with multiple E2-dependent ERα-binding regions. Here, we show E2-dependent super enhancer-associated characteristics and suggest contact between the distal enhancer and the Igf1 TSS. We hypothesized that this distal super-enhancer region controls E2-responsive induction of uterine Igf1 transcripts. We deleted 430 bp, encompassing one of the ERα-binding sites, thereby disrupting interactions of the enhancer with gene-regulatory factors. As a result, E2-mediated induction of mouse uterine Igf1 mRNA is completely eliminated, whereas hepatic Igf1 expression remains unaffected. This highlights the central role of a distal enhancer in the assembly of the factors necessary for E2-dependent interaction with the Igf1 TSS and induction of uterus-specific Igf1 transcription. Of note, loss of the enhancer did not affect fertility or uterine growth responses. Deletion of uterine Igf1 in a PgrCre;Igf1f/f model decreased female fertility but did not impact the E2-induced uterine growth response. Moreover, E2-dependent activation of uterine IGF1 signaling was not impaired by disrupting the distal enhancer or by deleting the coding transcript. This indicated a role for systemic IGF1, suggested that other growth mediators drive uterine response to E2, and suggested that uterine-derived IGF1 is essential for reproductive success. Our findings elucidate the role of a super enhancer in Igf1 regulation and uterine growth.
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Lin, Kwang-Huei, Won-Jing Wang, Yi-Hsin Wu, and Sheue-Yann Cheng. "Activation of Antimetastatic Nm23-H1 Gene Expression by Estrogen and Its α-Receptor." Endocrinology 143, no. 2 (February 1, 2002): 467–75. http://dx.doi.org/10.1210/endo.143.2.8620.
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Abstract Metastasis of various malignant cells is inversely related to the abundance of the Nm23-H1 protein. The role of estrogens in tumor metastasis has now been investigated by examining the effect of E2 on the expression of the Nm23-H1 gene. Three human breast carcinoma cell lines, in which endogenous ERα is expressed at different levels, were used as a tool to assess the role of ERα in Nm23-H1 gene-mediated metastasis. E2 induced time-dependent increases in the abundance of Nm23-H1 mRNA and protein, with the extent of these effects correlating with the level of expression of ERα. E2 induced a marked decrease in the invasive activity of MCF-7 and BT-474 cells but had no effect on BCM-1 cells, which had virtually no ERα. Consistent with these results, the ER-mediated Nm23-H1 promoter activity was inhibited 3-fold by the E2 antagonist, ICI 182,780. Deletion analysis of the promoter region of the Nm23-H1 gene identified a positive estrogen-responsive element located in −108/−94. ER protein bound specifically to the −108/−79 fragment with high avidity. These results indicate that E2, acting through ERα, activated transcription of the Nm23-H1 gene via a positive estrogen-responsive element in the promoter region of the gene. These results suggest that E2 could suppress tumor metastasis by activating the expression of the Nm23-H1 gene.
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Jutzi, Jonas S., Ruzhica Bogeska, Gorica Nikoloski, Corina A. Schmid, Thalia S. Seeger, Frank Stegelmann, Sven Schwemmers, et al. "MPN patients harbor recurrent truncating mutations in transcription factor NF-E2." Journal of Experimental Medicine 210, no. 5 (April 15, 2013): 1003–19. http://dx.doi.org/10.1084/jem.20120521.
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The molecular etiology of myeloproliferative neoplasms (MPNs) remains incompletely understood, despite recent advances incurred through the discovery of several different mutations in MPN patients. We have recently described overexpression of the transcription factor NF-E2 in MPN patients and shown that elevated NF-E2 levels in vivo cause an MPN phenotype and predispose to leukemic transformation in transgenic mice. We report the presence of acquired insertion and deletion mutations in the NF-E2 gene in MPN patients. These result in truncated NF-E2 proteins that enhance wild-type (WT) NF-E2 function and cause erythrocytosis and thrombocytosis in a murine model. NF-E2 mutant cells acquire a proliferative advantage, witnessed by clonal dominance over WT NF-E2 cells in MPN patients. Our data underscore the role of increased NF-E2 activity in the pathophysiology of MPNs.
Dissertations / Theses on the topic "E2 gene deletion"
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Šepetienė, Agnė. "Intraepiteliniai gimdos kaklelio pokyčiai ir žmogaus papilomos viruso integracija." Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2011. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2011~D_20110307_144709-15522.
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Disertacijoje nagrinėjama sąsaja tarp žmogaus papilomos viruso (ŽPV) integracijos į gimdos kaklelio epitelio ląstelių genomą ir intraepitelinių gimdos kaklelio pokyčių. Pagrindinis darbo tikslas – nustatyti, kaip 16 tipo ŽPV DNR integracijos laipsnis (ŽPV E2 geno iškrita) susijęs su intraepiteliniais gimdos kaklelio pokyčiais. Ištyrus 253 moteris nustatyta, kad dauguma moterų buvo infekuotos 16 tipo ŽPV. Dažniausiai nustatyta II laipsnio šio tipo ŽPV integracija. Statistiškai reikšmingo skirtumo analizuojant sąsajas tarp ŽPV E2 geno integracijos pobūdžio ir intraepitelinių gimdos kaklelio pokyčių laipsnio nenustatyta. Tai, kad integruotų 16 tipo ŽPV formų nustatyta esant nežymių arba net nesant intraepitelinių gimdos kaklelio pokyčių, rodo, jog viruso integracija yra ankstyvasis kancerogenezės įvykis. Pažymėtina, kad pakartotinio patikrinimo metu 50 proc. ŽPV infekuotų moterų konstatuota mRNR raiška, kas rodo besitęsiančią aktyvią ŽPV infekciją. Atliktas tyrimas yra svarbus gerinant patikros dėl gimdos kaklelio patologijos programas: derinant Pap testą ir ŽPV DNR bei kitų ŽPV žymenų nustatymą (mRNR, E2 geno iškrita) galima atrinkti infekuotas ŽPV moteris, kurioms dar nėra klinikinių požymių, tačiau jos priklauso didelės rizikos susirgti gimdos kaklelio vėžiu grupei.This dissertation observes the association between human papillomavirus (HPV) integration into the host cell genome and cervical intraepithelial lesions. The aim of this study is to determine how the grade of HPV16 DNA integration into the host cell genome (HPV E2 gene deletion) is related to cervical intraepithelial lesions. 253 women were screened for HPV infection and the majority was diagnosed with HPV type 16. The most frequently determined was HPV grade II integration. No statistically significant difference was defined while analyzing the relations between the status of HPV E2 gene integration and the grade of cervical intraepithelial lesions. The fact that integration of HPV type 16 was determined in low grade cervical squamous intraepithelial lesions or in cases with no intraepithelial lesions shows that virus integration occurs at the early stage of carcinogenesis. It is noteworthy that during the follow-up (secondary visit after 6 month) 50% of HPV positive women were identified with mRNR expression which probably establishes the presence of persistent active HPV infection. The research provided is highly significant for improvement of cervical cancer screening programms. Adjusting Pap smear, HPV DNA detection and determination of other HPV biomarkers (such as E2 gene deletion mRNR), it becomes possible to separate out HPV positive women with no clinical signs, although, belonging to the of high risk group for cervical carcinoma developing.
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Šepetienė, Agnė. "Cervical intraepithelial lesions and integration of human papillomavirus." Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2011. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2011~D_20110307_144558-96943.
Full textAbstract:
This dissertation observes the association between human papillomavirus (HPV) integration into the host cell genome and cervical intraepithelial lesions. The aim of this study is to determine how the grade of HPV16 DNA integration into the host cell genome (HPV E2 gene deletion) is related to cervical intraepithelial lesions. 253 women were screened for HPV infection and the majority was diagnosed with HPV type 16. The most frequently determined was HPV grade II integration. No statistically significant difference was defined while analyzing the relations between the status of HPV E2 gene integration and the grade of cervical intraepithelial lesions. The fact that integration of HPV type 16 was determined in low grade cervical squamous intraepithelial lesions or in cases with no intraepithelial lesions shows that virus integration occurs at the early stage of carcinogenesis. It is noteworthy that during the follow-up (secondary visit after 6 month) 50% of HPV positive women were identified with mRNR expression which probably establishes the presence of persistent active HPV infection. The research provided is highly significant for improvement of cervical cancer screening programms. Adjusting Pap smear, HPV DNA detection and determination of other HPV biomarkers (such as E2 gene deletion mRNR), it becomes possible to separate out HPV positive women with no clinical signs, although, belonging to the of high risk group for cervical carcinoma developing.Disertacijoje nagrinėjama sąsaja tarp žmogaus papilomos viruso (ŽPV) integracijos į gimdos kaklelio epitelio ląstelių genomą ir intraepitelinių gimdos kaklelio pokyčių. Pagrindinis darbo tikslas – nustatyti, kaip 16 tipo ŽPV DNR integracijos laipsnis (ŽPV E2 geno iškrita) susijęs su intraepiteliniais gimdos kaklelio pokyčiais. Ištyrus 253 moteris nustatyta, kad dauguma moterų buvo infekuotos 16 tipo ŽPV. Dažniausiai nustatyta II laipsnio šio tipo ŽPV integracija. Statistiškai reikšmingo skirtumo analizuojant sąsajas tarp ŽPV E2 geno integracijos pobūdžio ir intraepitelinių gimdos kaklelio pokyčių laipsnio nenustatyta. Tai, kad integruotų 16 tipo ŽPV formų nustatyta esant nežymių arba net nesant intraepitelinių gimdos kaklelio pokyčių, rodo, jog viruso integracija yra ankstyvasis kancerogenezės įvykis. Pažymėtina, kad pakartotinio patikrinimo metu 50 proc. ŽPV infekuotų moterų konstatuota mRNR raiška, kas rodo besitęsiančią aktyvią ŽPV infekciją. Atliktas tyrimas yra svarbus gerinant patikros dėl gimdos kaklelio patologijos programas: derinant Pap testą ir ŽPV DNR bei kitų ŽPV žymenų nustatymą (mRNR, E2 geno iškrita) galima atrinkti infekuotas ŽPV moteris, kurioms dar nėra klinikinių požymių, tačiau jos priklauso didelės rizikos susirgti gimdos kaklelio vėžiu grupei.