Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA389743 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:p62 sustains a protumorigenic gene signature in melanoma opposing mRNA-dependent decay [SKMEL_6days]
| PRJNA389742 | ENA
Project description:p62 sustains a protumorigenic gene signature in melanoma opposing mRNA-dependent decay [UACC62_6days]
| PRJNA389744 | ENA
Project description:p62 sustains a protumorigenic gene signature in melanoma opposing mRNA-dependent decay [UACC62_3days]
| PRJNA389745 | ENA
Project description:p62 sustains a protumorigenic gene signature in melanoma opposing mRNA-dependent decay
| PRJNA389739 | ENA
Project description:mRNA decay factors regulate mRNA turnover by recruiting non-translating mRNAs and targeting them for degradation, yet it remains poorly understood how mRNA decay factors function in vivo to regulate specific cellular processes. Here we show that mRNA decay factors form cytoplasmic puncta in C. elegans neurons and have opposing roles in axon maintenance and regrowth. While the decapping enzymes DCAP-1/DCP1 and DCAP-2/DCP2 regulate developmental axon guidance and promote axon regrowth upon injury, the translational repressors CAR-1/LSM14 and CGH-1/DDX6 regulate axon maintenance and inhibit axon regrowth in adult animals. We identified mRNA targets of CAR-1 in neurons and found that the mitochondrial calcium uptake regulator micu-1 is repressed by CAR-1. We show that axon injury triggers a transient mitochondrial calcium influx via the MCU-1 uniporter that is more sustained in car-1 loss of function mutants. The enhanced axon regrowth and defective axon maintenance of car-1 mutants are dependent on MICU-1 function. Our results uncover specific roles for mRNA decay regulators in neurons and reveal a novel pathway that controls axon regrowth through mitochondrial calcium uptake.
2020-01-23 | GSE124714 | GEO
Project description:p62/SQSTM1 was identified as a modulator of metastatic genes selectively enriched in melanoma in autophagy independent manner. iTRAQ quantitative proteomic approach was performed in melanoma cell lines (SK-Mel-103 and UACC-62) deficient for p62 to identify downstream effectors of p62. Similar studies were performed for ATG5, a core component of autophagy, as a reference for autophagy-associated changes in protein abundance. Additionally, melanoma cells were subjected to affinity purification (AP-MS) to identify the interactors of p62. Overall, these studies underscore a novel unexpected role of p62 regulating the stability of prometastatic factors via the interaction with RNA Binding Proteins, thus leading to the inhibition of protein translation.
2022-02-28 | PXD006650 | Pride
Project description:p62/SQSTM1 was identified as a modulator of metastatic genes selectively enriched in melanoma in autophagy independent manner. iTRAQ quantitative proteomic approach was performed in melanoma cell lines (SK-Mel-103 and UACC-62) deficient for p62 to identify downstream effectors of p62. Similar studies were performed for ATG5, a core component of autophagy, as a reference for autophagy-associated changes in protein abundance. Additionally, melanoma cells were subjected to affinity purification (AP-MS) to identify the interactors of p62. Overall, these studies underscore a novel unexpected role of p62 regulating the stability of prometastatic factors via the interaction with RNA Binding Proteins, thus leading to the inhibition of protein translation.
2021-10-29 | PXD007000 | Pride
Project description:mRNA abundances are regulated by the opposing forces of transcription and decay, and yet how decay contributes to mRNA abundance regulation is largely unexplored. We addressed this question using genome-wide data on mRNA rates of abundance change, half-lives, and transcription rates of leaf cells responding to a transdifferentiation stimulusulus. Half-life regulation was common (22% of mRNAs underwent changes in half-life), but RNA abundance regulation by decay alone or by decay that supported transcriptional regulation was rare. Instead, most altered RNA half-lives opposed changes in transcription. Oppositionally regulated mRNAs were characterized by large changes in transcription and decay rates yet changes in mRNA abundances were either modest or undetectable, suggestive of RNA buffering. Oppositionally-regulated and buffered RNAs showed very similar dynamics, suggesting use of a common mechanism. The strongest contributions of RNA decay to RNA abundance regulation was in synergistically regulated transcripts, where rate changes in decay and transcription rates worked together to change RNA abundances.
2024-10-11 | GSE278544 | GEO
Project description:mRNA abundances are regulated by the opposing forces of transcription and decay, and yet how decay contributes to mRNA abundance regulation is largely unexplored. We addressed this question using genome-wide data on mRNA rates of abundance change, half-lives, and transcription rates of leaf cells responding to a transdifferentiation stimulusulus. Half-life regulation was common (22% of mRNAs underwent changes in half-life), but RNA abundance regulation by decay alone or by decay that supported transcriptional regulation was rare. Instead, most altered RNA half-lives opposed changes in transcription. Oppositionally regulated mRNAs were characterized by large changes in transcription and decay rates yet changes in mRNA abundances were either modest or undetectable, suggestive of RNA buffering. Oppositionally-regulated and buffered RNAs showed very similar dynamics, suggesting use of a common mechanism. The strongest contributions of RNA decay to RNA abundance regulation was in synergistically regulated transcripts, where rate changes in decay and transcription rates worked together to change RNA abundances.
2024-10-11 | GSE278543 | GEO
Project description:TTP-dependent mRNA decay in LPS-stimulated macrophages
| PRJNA139903 | ENA