Comparison of gene expression profiles of neonate rat cardiomyocytes (NRCMs) transfected with LacZ, 23k prolactin (PRL), or 16k PRL.
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE169063 | GEO | 2021/04/30
REPOSITORIES: GEO
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Project description:Comparison of gene expression profiles of neonate rat cardiomyocytes (NRCMs) transfected with LacZ, 23k prolactin (PRL), or 16k PRL.
| PRJNA715095 | ENA
Project description:The multifunctional protein tyrosine phosphatase PRL-1 (Gene Symbol: PTP4A1) has been identified as an important oncogene with roles in promoting cell proliferation, survival, migration, invasion, and metastasis. However, little is currently known about the signaling pathways through which it mediates its effects. We used Affymetrix Human Genome U133 Plus 2.0 arrays to examine the global molecular changes of gene expression occurring in response to stable PRL-1 overexpression in human embryonic kidney 293 (HEK293) cells. Total RNA was extracted from triplicate cultures of HEK293 cells stably overexpressing PRL-1 (HEK293-PRL-1) and HEK293 cells stably transfected with empty pcDNA4 vector (HEK293-Vector). Samples were hybridized to Affymetrix HG U133 Plus 2.0 microarrays (1 array per sample for a total of 6 arrays). One of the arrays hybridized with a PRL-1 transfected sample was excluded after qRT-PCR demonstrated that this sample did not exhibit increased PRL-1 expression over the level of the empty vector controls. The remaining 2 HEK293-PRL-1 samples both expressed PRL-1 at least 2-fold higher than any of the 3 empty vector controls.
2013-07-30 | E-GEOD-42586 | biostudies-arrayexpress
Project description:The protein tyrosine phosphatase PRL-1 (Gene Symbol: PTP4A1) has been identified as an important oncogene with roles in promoting cell proliferation, survival, migration, invasion, and metastasis. However, little is currently known about the signaling pathways through which it mediates its effects. Studies have shown a relationship between PRL-1 and the expression or activity levels of various molecules involved in integrin-mediated cell signaling. These integrin-responsive players can promote re-arrangements in the actin cytoskeleton that are central to cell motility, invasion, and metastasis. Therefore, to investigate the effects of PRL-1 overexpression in human embryonic kidney 293 (HEK293) cells, we used qRT-PCR to examine the expression levels of 184 genes which either were identified by microarray and proteomic analysis to be differentially expressed in response to PRL-1 or have known associations to integrin-mediated signaling, cytoskeletal remodeling, and/or cell motility. Total RNA was extracted from duplicate cultures of HEK293 cells stably overexpressing PRL-1 (HEK293-PRL-1) and HEK293 cells stably transfected with empty pcDNA4 vector (HEK293-Vector). Samples were analyzed using custom TaqMan Array 96-well Plates to examine the expression of 184 genes with known involvement in or association with signaling pathways related to integrin-mediated cell adhesion, cytoskeletal remodeling, and/or cell motility.
2013-07-30 | E-GEOD-42587 | biostudies-arrayexpress
Project description:The protein tyrosine phosphatase PRL-1 (Gene Symbol: PTP4A1) has been identified as an important oncogene with roles in promoting cell proliferation, survival, migration, invasion, and metastasis. However, little is currently known about the signaling pathways through which it mediates its effects. Studies have shown a relationship between PRL-1 and the expression or activity levels of various molecules involved in integrin-mediated cell signaling. These integrin-responsive players can promote re-arrangements in the actin cytoskeleton that are central to cell motility, invasion, and metastasis. Therefore, to investigate the effects of PRL-1 overexpression in human embryonic kidney 293 (HEK293) cells, we used qRT-PCR to examine the expression levels of 184 genes which either were identified by microarray and proteomic analysis to be differentially expressed in response to PRL-1 or have known associations to integrin-mediated signaling, cytoskeletal remodeling, and/or cell motility.
2013-07-30 | GSE42587 | GEO
Project description:The multifunctional protein tyrosine phosphatase PRL-1 (Gene Symbol: PTP4A1) has been identified as an important oncogene with roles in promoting cell proliferation, survival, migration, invasion, and metastasis. However, little is currently known about the signaling pathways through which it mediates its effects. We used Affymetrix Human Genome U133 Plus 2.0 arrays to examine the global molecular changes of gene expression occurring in response to stable PRL-1 overexpression in human embryonic kidney 293 (HEK293) cells.
2013-07-30 | GSE42586 | GEO
Project description:The timing of behavior under natural light-dark conditions is a function of circadian clocks and photic input pathways. Yet a mechanistic understanding of how these pathways collaborate in animals is lacking. Here we demonstrate in Drosophila that the Phosphatase of Regenerating Liver-1 (PRL-1) sets period length and behavioral phase gated by photic signals. PRL-1 knockdown in PDF clock neurons dramatically lengthens circadian period. PRL-1 mutants exhibit allele-specific interactions with the light- and clock-regulated gene timeless (tim). Moreover, we show that PRL-1 promotes TIM accumulation and dephosphorylation. Interestingly, the PRL-1 mutant period lengthening is suppressed in constant light and PRL-1 mutants display a delayed phase under short, but not long, photoperiod conditions. Thus, our studies reveal that PRL-1 dependent dephosphorylation of TIM is a core mechanism of the clock that sets period length and phase in darkness, enabling the behavioral adjustment to changing day-night cycles.
2020-11-11 | PXD020986 | Pride
Project description:PRL-3 is an oncogenic phosphatase, which is expressed at a higher level in malignant plasma cells from multiple myeloma patients than in plasma cells from healthy donors and high expression is associated with a poor prognosis. We overexpressed PRL-3 in a multiple myeloma cell line and our goal was to find signaling pathways regulated by PRL-3 in myeloma cells.
2021-07-01 | E-MTAB-10436 | biostudies-arrayexpress
Project description:Transcriptional control by gonadal hormone nuclear receptors is the foundation for sex-dependent physiological processes, including pain. Our current findings point to sex-dependent translation control as a new mechanism for sexual dimorphisms in pain. We show that hindpaw or spinal administration of exogenous prolactin (PRL) induces thermal and mechanical hyperalgesia in a female-selective fashion. Unexpectedly, PCR and transcriptomic analysis of hindpaw and dorsal root ganglion (DRG) tissues reveal no differences in PRL receptor (Prlr) mRNA between sexes. Variance in overall hindpaw and DRG transcriptomes between females and males were minor. We find that Prlr mRNA and protein is mainly expressed by peptidergic nociceptors as shown by profiling using Prlr reporter mice and electrophysiology, but there are far more peptidergic neurons with functional Prlr in females than in males. In line with this, exogenous PRL increased excitability only in female neurons. Moreover, in male DRG neurons, 6-24 hr estrogen exposure establishes PRL sensitivity in Prlr mRNA+ male neurons that do not show PRL responses under other conditions. PRL-induced behavioral hypersensitivity as well as sensitivity to PRL in female DRG neurons can be ablated by treatment with cap-dependent translation inhibitor 4EGI-1. Spinal cord immunohistochemistry of Prlr reporter mice highlight that Prlr protein is only found in female DRG neurons, but Prlr mRNA localizes to central terminals of male and female sensory neurons. Based on these findings, we propose a novel mechanism for sex-dependent regulation Prlr mRNA translation that renders female DRG neurons uniquely responsive to PRL.
2019-03-01 | GSE121645 | GEO
Project description:Transcriptional control by gonadal hormone nuclear receptors is the foundation for sex-dependent physiological processes, including pain. Our current findings point to sex-dependent translation control as a new mechanism for sexual dimorphisms in pain. We show that hindpaw or spinal administration of exogenous prolactin (PRL) induces thermal and mechanical hyperalgesia in a female-selective fashion. Unexpectedly, PCR and transcriptomic analysis of hindpaw and dorsal root ganglion (DRG) tissues reveal no differences in PRL receptor (Prlr) mRNA between sexes. Variance in overall hindpaw and DRG transcriptomes between females and males were minor. We find that Prlr mRNA and protein is mainly expressed by peptidergic nociceptors as shown by profiling using Prlr reporter mice and electrophysiology, but there are far more peptidergic neurons with functional Prlr in females than in males. In line with this, exogenous PRL increased excitability only in female neurons. Moreover, in male DRG neurons, 6-24 hr estrogen exposure establishes PRL sensitivity in Prlr mRNA+ male neurons that do not show PRL responses under other conditions. PRL-induced behavioral hypersensitivity as well as sensitivity to PRL in female DRG neurons can be ablated by treatment with cap-dependent translation inhibitor 4EGI-1. Spinal cord immunohistochemistry of Prlr reporter mice highlight that Prlr protein is only found in female DRG neurons, but Prlr mRNA localizes to central terminals of male and female sensory neurons. Based on these findings, we propose a novel mechanism for sex-dependent regulation Prlr mRNA translation that renders female DRG neurons uniquely responsive to PRL.
2023-11-17 | GSE161826 | GEO
Project description:In order to investigate the role of PRL-3 in the leukemogenesis, we transfected a control vector (pEGFP) and (human) PRL-3 gene into an acute myeloid leukemia (AML) cell line TF-1, respectively. After drug selection and FACS sorting, we established TF1-pEGFP and TF1-hPRL-3 isogenic cell lines. In vitro and in vivo experiments were conducted to characterized this pair of isogenic cell lines. Results provided insight into the molecular basis of PRL-3 in contributing the development of AML.
2017-01-11 | GSE64872 | GEO