Eintrag weiter verarbeiten
Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation
Gespeichert in:
| Zeitschriftentitel: | Clinical Epigenetics |
|---|---|
| Personen und Körperschaften: | , , , |
| In: | Clinical Epigenetics, 2, 2011, 2, S. 331-338 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Springer Science and Business Media LLC
|
| Schlagwörter: |
| author_facet |
Tell, Robert Wang, Q. Tian Blunier, Adam Benya, Richard V. Tell, Robert Wang, Q. Tian Blunier, Adam Benya, Richard V. |
|---|---|
| author |
Tell, Robert Wang, Q. Tian Blunier, Adam Benya, Richard V. |
| spellingShingle |
Tell, Robert Wang, Q. Tian Blunier, Adam Benya, Richard V. Clinical Epigenetics Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation Genetics (clinical) Developmental Biology Genetics Molecular Biology |
| author_sort |
tell, robert |
| spelling |
Tell, Robert Wang, Q. Tian Blunier, Adam Benya, Richard V. 1868-7075 1868-7083 Springer Science and Business Media LLC Genetics (clinical) Developmental Biology Genetics Molecular Biology http://dx.doi.org/10.1007/s13148-011-0027-5 <jats:title>Abstract</jats:title> <jats:p>Epithelial cells lining the adult colon do not normally express gastrin-releasing peptide (GRP) or its receptor (GRPR). In contrast, GRP/GRPR can be aberrantly expressed in human colorectal cancer (CRC) including Caco-2 cells. We have previously shown that GRPR activation results in the up-regulation of HP1β, an epigenetic modifier of gene transcription. The aim of this study was to identify the genes whose expression is altered by HP1β subsequent to GRPR activation. We determined HP1β binding positions throughout the genome using chromatin immunoprecipitation followed by massively parallel DNA sequencing (ChIP-seq). After exposure to GRP, we identified 9,625 genomic positions occupied by HP1β. We performed gene microarray analysis on Caco-2 cells in the absence and presence of a GRPR specific antagonist as well as siRNA to HP1β. The expression of 97 genes was altered subsequent to GRPR antagonism, while the expression of 473 genes was altered by HP1β siRNA exposure. When these data were evaluated in concert with our ChIP-seq findings, 9 genes showed evidence of possible altered expression as a function of GRPR signaling via HP1β. Of these, genomic PCR of immunoprecipitated chromatin demonstrated that GRPR signaling affected the expression of IL1RAPL2, FAM13A, GBE1, PLK3, and SLCO1B3. These findings provide the first evidence by which GRPR aberrantly expressed in CRC might affect tumor progression.</jats:p> Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation Clinical Epigenetics |
| doi_str_mv |
10.1007/s13148-011-0027-5 |
| facet_avail |
Online Free |
| finc_class_facet |
Biologie |
| format |
ElectronicArticle |
| fullrecord |
blob:ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTAwNy9zMTMxNDgtMDExLTAwMjctNQ |
| id |
ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTAwNy9zMTMxNDgtMDExLTAwMjctNQ |
| institution |
DE-D275 DE-Bn3 DE-Brt1 DE-Zwi2 DE-D161 DE-Gla1 DE-Zi4 DE-15 DE-Pl11 DE-Rs1 DE-105 DE-14 DE-Ch1 DE-L229 |
| imprint |
Springer Science and Business Media LLC, 2011 |
| imprint_str_mv |
Springer Science and Business Media LLC, 2011 |
| issn |
1868-7075 1868-7083 |
| issn_str_mv |
1868-7075 1868-7083 |
| language |
English |
| mega_collection |
Springer Science and Business Media LLC (CrossRef) |
| match_str |
tell2011identificationofchipseqmappedtargetsofhp1bduetobombesingrpreceptoractivation |
| publishDateSort |
2011 |
| publisher |
Springer Science and Business Media LLC |
| recordtype |
ai |
| record_format |
ai |
| series |
Clinical Epigenetics |
| source_id |
49 |
| title |
Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation |
| title_unstemmed |
Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation |
| title_full |
Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation |
| title_fullStr |
Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation |
| title_full_unstemmed |
Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation |
| title_short |
Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation |
| title_sort |
identification of chip-seq mapped targets of hp1β due to bombesin/grp receptor activation |
| topic |
Genetics (clinical) Developmental Biology Genetics Molecular Biology |
| url |
http://dx.doi.org/10.1007/s13148-011-0027-5 |
| publishDate |
2011 |
| physical |
331-338 |
| description |
<jats:title>Abstract</jats:title>
<jats:p>Epithelial cells lining the adult colon do not normally express gastrin-releasing peptide (GRP) or its receptor (GRPR). In contrast, GRP/GRPR can be aberrantly expressed in human colorectal cancer (CRC) including Caco-2 cells. We have previously shown that GRPR activation results in the up-regulation of HP1β, an epigenetic modifier of gene transcription. The aim of this study was to identify the genes whose expression is altered by HP1β subsequent to GRPR activation. We determined HP1β binding positions throughout the genome using chromatin immunoprecipitation followed by massively parallel DNA sequencing (ChIP-seq). After exposure to GRP, we identified 9,625 genomic positions occupied by HP1β. We performed gene microarray analysis on Caco-2 cells in the absence and presence of a GRPR specific antagonist as well as siRNA to HP1β. The expression of 97 genes was altered subsequent to GRPR antagonism, while the expression of 473 genes was altered by HP1β siRNA exposure. When these data were evaluated in concert with our ChIP-seq findings, 9 genes showed evidence of possible altered expression as a function of GRPR signaling via HP1β. Of these, genomic PCR of immunoprecipitated chromatin demonstrated that GRPR signaling affected the expression of IL1RAPL2, FAM13A, GBE1, PLK3, and SLCO1B3. These findings provide the first evidence by which GRPR aberrantly expressed in CRC might affect tumor progression.</jats:p> |
| container_issue |
2 |
| container_start_page |
331 |
| container_title |
Clinical Epigenetics |
| container_volume |
2 |
| format_de105 |
Article, E-Article |
| format_de14 |
Article, E-Article |
| format_de15 |
Article, E-Article |
| format_de520 |
Article, E-Article |
| format_de540 |
Article, E-Article |
| format_dech1 |
Article, E-Article |
| format_ded117 |
Article, E-Article |
| format_degla1 |
E-Article |
| format_del152 |
Buch |
| format_del189 |
Article, E-Article |
| format_dezi4 |
Article |
| format_dezwi2 |
Article, E-Article |
| format_finc |
Article, E-Article |
| format_nrw |
Article, E-Article |
| _version_ |
1792326089536700433 |
| geogr_code |
not assigned |
| last_indexed |
2024-03-01T12:15:24.894Z |
| geogr_code_person |
not assigned |
| openURL |
url_ver=Z39.88-2004&ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fvufind.svn.sourceforge.net%3Agenerator&rft.title=Identification+of+ChIP-seq+mapped+targets+of+HP1%CE%B2+due+to+bombesin%2FGRP+receptor+activation&rft.date=2011-08-01&genre=article&issn=1868-7083&volume=2&issue=2&spage=331&epage=338&pages=331-338&jtitle=Clinical+Epigenetics&atitle=Identification+of+ChIP-seq+mapped+targets+of+HP1%CE%B2+due+to+bombesin%2FGRP+receptor+activation&aulast=Benya&aufirst=Richard+V.&rft_id=info%3Adoi%2F10.1007%2Fs13148-011-0027-5&rft.language%5B0%5D=eng |
| SOLR | |
| _version_ | 1792326089536700433 |
| author | Tell, Robert, Wang, Q. Tian, Blunier, Adam, Benya, Richard V. |
| author_facet | Tell, Robert, Wang, Q. Tian, Blunier, Adam, Benya, Richard V., Tell, Robert, Wang, Q. Tian, Blunier, Adam, Benya, Richard V. |
| author_sort | tell, robert |
| container_issue | 2 |
| container_start_page | 331 |
| container_title | Clinical Epigenetics |
| container_volume | 2 |
| description | <jats:title>Abstract</jats:title> <jats:p>Epithelial cells lining the adult colon do not normally express gastrin-releasing peptide (GRP) or its receptor (GRPR). In contrast, GRP/GRPR can be aberrantly expressed in human colorectal cancer (CRC) including Caco-2 cells. We have previously shown that GRPR activation results in the up-regulation of HP1β, an epigenetic modifier of gene transcription. The aim of this study was to identify the genes whose expression is altered by HP1β subsequent to GRPR activation. We determined HP1β binding positions throughout the genome using chromatin immunoprecipitation followed by massively parallel DNA sequencing (ChIP-seq). After exposure to GRP, we identified 9,625 genomic positions occupied by HP1β. We performed gene microarray analysis on Caco-2 cells in the absence and presence of a GRPR specific antagonist as well as siRNA to HP1β. The expression of 97 genes was altered subsequent to GRPR antagonism, while the expression of 473 genes was altered by HP1β siRNA exposure. When these data were evaluated in concert with our ChIP-seq findings, 9 genes showed evidence of possible altered expression as a function of GRPR signaling via HP1β. Of these, genomic PCR of immunoprecipitated chromatin demonstrated that GRPR signaling affected the expression of IL1RAPL2, FAM13A, GBE1, PLK3, and SLCO1B3. These findings provide the first evidence by which GRPR aberrantly expressed in CRC might affect tumor progression.</jats:p> |
| doi_str_mv | 10.1007/s13148-011-0027-5 |
| facet_avail | Online, Free |
| finc_class_facet | Biologie |
| format | ElectronicArticle |
| format_de105 | Article, E-Article |
| format_de14 | Article, E-Article |
| format_de15 | Article, E-Article |
| format_de520 | Article, E-Article |
| format_de540 | Article, E-Article |
| format_dech1 | Article, E-Article |
| format_ded117 | Article, E-Article |
| format_degla1 | E-Article |
| format_del152 | Buch |
| format_del189 | Article, E-Article |
| format_dezi4 | Article |
| format_dezwi2 | Article, E-Article |
| format_finc | Article, E-Article |
| format_nrw | Article, E-Article |
| geogr_code | not assigned |
| geogr_code_person | not assigned |
| id | ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTAwNy9zMTMxNDgtMDExLTAwMjctNQ |
| imprint | Springer Science and Business Media LLC, 2011 |
| imprint_str_mv | Springer Science and Business Media LLC, 2011 |
| institution | DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229 |
| issn | 1868-7075, 1868-7083 |
| issn_str_mv | 1868-7075, 1868-7083 |
| language | English |
| last_indexed | 2024-03-01T12:15:24.894Z |
| match_str | tell2011identificationofchipseqmappedtargetsofhp1bduetobombesingrpreceptoractivation |
| mega_collection | Springer Science and Business Media LLC (CrossRef) |
| physical | 331-338 |
| publishDate | 2011 |
| publishDateSort | 2011 |
| publisher | Springer Science and Business Media LLC |
| record_format | ai |
| recordtype | ai |
| series | Clinical Epigenetics |
| source_id | 49 |
| spelling | Tell, Robert Wang, Q. Tian Blunier, Adam Benya, Richard V. 1868-7075 1868-7083 Springer Science and Business Media LLC Genetics (clinical) Developmental Biology Genetics Molecular Biology http://dx.doi.org/10.1007/s13148-011-0027-5 <jats:title>Abstract</jats:title> <jats:p>Epithelial cells lining the adult colon do not normally express gastrin-releasing peptide (GRP) or its receptor (GRPR). In contrast, GRP/GRPR can be aberrantly expressed in human colorectal cancer (CRC) including Caco-2 cells. We have previously shown that GRPR activation results in the up-regulation of HP1β, an epigenetic modifier of gene transcription. The aim of this study was to identify the genes whose expression is altered by HP1β subsequent to GRPR activation. We determined HP1β binding positions throughout the genome using chromatin immunoprecipitation followed by massively parallel DNA sequencing (ChIP-seq). After exposure to GRP, we identified 9,625 genomic positions occupied by HP1β. We performed gene microarray analysis on Caco-2 cells in the absence and presence of a GRPR specific antagonist as well as siRNA to HP1β. The expression of 97 genes was altered subsequent to GRPR antagonism, while the expression of 473 genes was altered by HP1β siRNA exposure. When these data were evaluated in concert with our ChIP-seq findings, 9 genes showed evidence of possible altered expression as a function of GRPR signaling via HP1β. Of these, genomic PCR of immunoprecipitated chromatin demonstrated that GRPR signaling affected the expression of IL1RAPL2, FAM13A, GBE1, PLK3, and SLCO1B3. These findings provide the first evidence by which GRPR aberrantly expressed in CRC might affect tumor progression.</jats:p> Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation Clinical Epigenetics |
| spellingShingle | Tell, Robert, Wang, Q. Tian, Blunier, Adam, Benya, Richard V., Clinical Epigenetics, Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation, Genetics (clinical), Developmental Biology, Genetics, Molecular Biology |
| title | Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation |
| title_full | Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation |
| title_fullStr | Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation |
| title_full_unstemmed | Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation |
| title_short | Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation |
| title_sort | identification of chip-seq mapped targets of hp1β due to bombesin/grp receptor activation |
| title_unstemmed | Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation |
| topic | Genetics (clinical), Developmental Biology, Genetics, Molecular Biology |
| url | http://dx.doi.org/10.1007/s13148-011-0027-5 |