Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Preanalytical impacts on protein stability by IHC evaluation

ABSTRACT: Preanalytical impacts on protein stability by IHC evaluation

PROVIDER: PRJNA701506 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Breast tumor specific mutation in GATA3 impacts protein stability and genomic location

Project description:The transcription factor GATA3 is a favorable prognostic indicator in estrogen receptor-M-NM-1 (ERM-NM-1)-positive breast tumors in which it participates with ERa and FOXA1 in a complex transcriptional regulatory program driving tumor growth. Paradoxically, GATA3 mutations are frequent in breast cancer and have been classified as drivers. To elucidate the contribution(s) of GATA3 alterations to oncogenesis, we studied two breast cancer cell lines, MCF7, which carries a heterozygous frameshift mutation in the second zinc finger of GATA3, and T47D, wild-type at this locus. Heterozygosity for the truncating mutation conferred protection from regulated turnover of GATA3, ERa and FOXA1 following estrogen stimulation. Thus, mutant GATA3 uncouples protein-level regulation of master regulatory transcription factors from hormone action. Consistent with increased protein stability, ChIP-seq profiling identified stronger accumulation of GATA3 in cells bearing the mutation, albeit with a similar distribution across the genome. We propose that this specific, cancer-derived mutation in GATA3 deregulates physiologic protein turnover, stabilizes GATA3 binding across the genome and modulates the response of mammary epithelial cells to hormone signaling, thus conferring a selective growth advantage. Genome-wide mapping of GATA3 in two cell lines. There were two biological replicates and unchipped (input) DNA was used as reference.

2014-04-01 | E-GEOD-51274 | biostudies-arrayexpress

Breast tumor specific mutation in GATA3 impacts protein stability and genomic location

Project description:The transcription factor GATA3 is a favorable prognostic indicator in estrogen receptor-α (ERα)-positive breast tumors in which it participates with ERa and FOXA1 in a complex transcriptional regulatory program driving tumor growth. Paradoxically, GATA3 mutations are frequent in breast cancer and have been classified as drivers. To elucidate the contribution(s) of GATA3 alterations to oncogenesis, we studied two breast cancer cell lines, MCF7, which carries a heterozygous frameshift mutation in the second zinc finger of GATA3, and T47D, wild-type at this locus. Heterozygosity for the truncating mutation conferred protection from regulated turnover of GATA3, ERa and FOXA1 following estrogen stimulation. Thus, mutant GATA3 uncouples protein-level regulation of master regulatory transcription factors from hormone action. Consistent with increased protein stability, ChIP-seq profiling identified stronger accumulation of GATA3 in cells bearing the mutation, albeit with a similar distribution across the genome. We propose that this specific, cancer-derived mutation in GATA3 deregulates physiologic protein turnover, stabilizes GATA3 binding across the genome and modulates the response of mammary epithelial cells to hormone signaling, thus conferring a selective growth advantage.

2014-04-01 | GSE51274 | GEO

Preanalytical Impacts on Protein Detection by HumanMap assay

Project description:Preanalytical Impacts on Protein Detection by HumanMap assay

| PRJNA701505 | ENA

Evaluation of Tn5 protein fusions suitable for GET-seq

Project description:Evaluation of Tn5 protein fusions suitable for GET-seq

| PRJEB40722 | ENA

The AMBRA1 E3 ligase adaptor regulates Cyclin D protein stability

Project description:The AMBRA1 E3 ligase adaptor regulates Cyclin D protein stability

| PRJNA670881 | ENA

Protein stability buffers the cost of translation attenuation following eIF2⍺ phosphorylation

Project description:Protein stability buffers the cost of translation attenuation following eIF2⍺ phosphorylation

| PRJNA657554 | ENA

Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis.

Project description:Prep1 is a tumor-suppressor, whereas Meis1 is an oncogene. We show that to perform these activities in MEFs both proteins competitively hetero-dimerize with Pbx1. Meis1 alone transforms Prep1-deficient fibroblasts while Prep1 overexpression inhibits Meis1 tumorigenicity. Pbx1 can therefore alternatively act as oncogene or tumor-suppressor. Prep1 post-translationally controls the level of Meis1 decreasing its stability by sequestering Pbx1. The different levels of Meis1 and the presence of Prep1 are followed at the transcriptional level by the induction of specific transcriptional signatures. The decrease of Meis1 prevents Meis1 interaction with Ddx3x and Ddx5, which are essential for Meis1 tumorigenesis, and modifies the growth promoting DNA binding landscape of Meis1 to the growth controlling landscape of Prep1. Hence the key feature of Prep1 tumor inhibiting activity is the control of Meis1 stability. Examination of Prep1 and Meis1 in three cell type

2014-03-05 | E-GEOD-54221 | biostudies-arrayexpress

Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis [hP]

2016-06-01 | E-GEOD-58802 | biostudies-arrayexpress

Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis

Project description:Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis

| PRJNA324117 | ENA

The AMBRA1 E3 ligase adaptor regulates Cyclin D protein stability [U2OS cells]

Project description:The AMBRA1 E3 ligase adaptor regulates Cyclin D protein stability [U2OS cells]

| PRJNA670897 | ENA