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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression Data from chemical induced tumors obtained from NDR1+/+, NDR1+/- and NDR1-/- mice

ABSTRACT: Loss and heterozygosity for NDR1 predisposes mice to T-cell lymphoma development. To analyze mechanisms of tumor development in these mice chemically (ENU)-induced tumors were collected and RNA was extracted. Tumors were collected from mice upon tumor development or 9 months after ENU treatment. Tumors were flash frozen and parts of the tumors were analyzed for RNA, proteins and histology.

ORGANISM(S): Mus musculus

SUBMITTER: Brian Hemmings

PROVIDER: E-GEOD-21902 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Ablation of the kinase NDR1 predisposes mice to the development of T cell lymphoma.

Cornils Hauke H Stegert Mario R MR Hergovich Alexander A Hynx Debby D Schmitz Debora D Dirnhofer Stephan S Hemmings Brian A BA

Science signaling 20100615 126

Defective apoptosis contributes to the development of various human malignancies. The kinases nuclear Dbf2-related 1 (NDR1) and NDR2 mediate apoptosis downstream of the tumor suppressor proteins RASSF1A (Ras association domain family member 1A) and MST1 (mammalian Ste20-like kinase 1). To further analyze the role of NDR1 in apoptosis, we generated NDR1-deficient mice. Although NDR1 is activated by both intrinsic and extrinsic proapoptotic stimuli, which indicates a role for NDR1 in regulating ap ...[more]

PMID: 20551432

Similar Datasets

Expression Data from chemical induced tumors obtained from NDR1+/+, NDR1+/- and NDR1-/- mice

Project description:Loss and heterozygosity for NDR1 predisposes mice to T-cell lymphoma development. To analyze mechanisms of tumor development in these mice chemically (ENU)-induced tumors were collected and RNA was extracted.

2010-06-16 | GSE21902 | GEO

PTP1B deficiency effect on mammary gland development and differentiation

Project description:Analysis of protein tyrosine phosphatase 1B (PTP1B) deficient mammary glands from nulliparous mice at estrous and pregnancy day 3, 7, 10 and 15. We used a genetically ablated PTP1B mouse model to gain a deeper knowledge of the role PTP1B plays in mammary gland development and to define the mechanism regulated by this phosphatase. Results provide insight into the role of PTP1B in mammary gland development and differentiation. Mouse mammary glands were isolated from PTP1B -/- and PTP1B +/+ nulliparous mice at estrous and pregnancy day 3, 7, 10 and 15 for RNA extraction and hybridization on Affymetrix microarrays.

2012-10-23 | E-GEOD-41768 | biostudies-arrayexpress

Primary TNBC tumor in the presence or absence of SHP2

Project description:The first bona fide PTP proto-oncogene was the Src-homology 2 domain-containing phosphatase SHP2 (encoded by PTPN11), an ubiquitously expressed PTP that transduces mitogenic, pro-survival, cell fate and/or pro-migratory signals from numerous growth factor-, cytokine- and extracellular matrix receptors. In malignancies, SHP2 is hyperactivated either downstream of oncoproteins or by mutations.We provide analysis of a primary triple-negative breast tumor grown as xenografts in the presence or absence of SHP2 for 30 days. A primary triple-negative breast tumor (BT8) was transduced with a doxycycline-inducible lentiviral vector expressing a CTRL miR or SHP2 miR1 or SHP2 miR2. Cells from each group were injected in immunodeficient mice and after tumor development, the knockdown of SHP2 was induced for 30 days in vivo. At day 30, tumors were dissected and RNA isolated for gene expression analysis.

2012-01-16 | E-GEOD-35118 | biostudies-arrayexpress

BT474 tumors in the presence or absence of SHP2

Project description:The first bona fide PTP proto-oncogene was the Src-homology 2 domain-containing phosphatase SHP2 (encoded by PTPN11), an ubiquitously expressed PTP that transduces mitogenic, pro-survival, cell fate and/or pro-migratory signals from numerous growth factor-, cytokine- and extracellular matrix receptors. In malignancies, SHP2 is hyperactivated either downstream of oncoproteins or by mutations.We provide analysis of the breast cancer cells BT474 grown as xenografts in the presence or absence of SHP2 for 30 days. The HER2-postive breast cancer cell line BT474 was transduced with a doxycycline-inducible lentiviral vector expressing a CTRL miR or SHP2 miR1 or SHP2 miR2. Cells from each group were injected in imuunodeficinet mice and after tumor development, the knockdown of SHP2 was induced for 30 days in vivo. At day 30, tumors were dissected and RNA isolated for gene expression analysis.

2011-12-20 | E-GEOD-34523 | biostudies-arrayexpress

Mus musculus

Project description:Expression Data from chemical induced tumors obtained from NDR1+/+, NDR1+/- and NDR1-/- mice

| PRJNA126819 | ENA

Loss of NDR1/2 kinases impairs endomembrane trafficking and ATG9A localisation, reduces autophagy and leads to neurodegeneration

Project description:Autophagy is essential for neuronal development and its deregulation contributes to neurodegenerative diseases. NDR1 and NDR2 are highly conserved kinases implicated in neuronal development, mitochondrial health and autophagy, but how they affect mammalian brain development in vivo is not known. Using single and double Ndr1/2 knockout mouse models we show that, dual, but not individual loss of Ndr1/2 in neurons causes neurodegeneration during brain development, but also in adult mice. Proteomic and phosphoproteomic comparisons between Ndr1/2 knockout and control brains revealed novel kinase substrates and indicated that endocytosis is significantly affected in the absence of NDR1/2. We validated the endocytic protein, Raph1/Lpd1 as a novel NDR1/2 substrate and showed that both NDR1/2 and Raph1 are critical for endocytosis and membrane recycling. In NDR1/2 knockout brains, we observed prominent accumulation of transferrin receptor, p62 and ubiquitinated proteins, indicative of a major impairment of protein homeostasis. Furthermore, the levels of LC3-positive autophagosomes were reduced in knockout neurons, implying that reduced autophagy efficiency mediates p62 accumulation and neurotoxicity. Mechanistically, pronounced mislocalisation of the transmembrane autophagy protein ATG9A at the neuronal periphery, impaired axonal ATG9A trafficking and increased ATG9A surface levels further confirm defects in membrane trafficking and could underlie the impairment in autophagy. We provide novel insight into the roles of NDR1/2 kinases in maintaining neuronal health.

2022-11-21 | PXD035566 | Pride

PRC1 coordinates timing of sexual differentiation of female primordial germ cells

Project description:In mammals, sex differentiation of primordial germ cells (PGCs) is determined by extrinsic cues from the environment1. In female PGCs, expression of Stimulated by retinoic acid 8 (Stra8) and meiosis are induced in response to retinoic acid (RA) provided by the mesonephroi2-4. Given the widespread role of RA signaling during development8,9, the molecular mechanism specifying the competence of PGCs to timely express Stra8 and enter meiosis are unknown2,10. Here we identify gene dosage dependent roles in PGC development for Ring1 and Rnf2, two central components of the Polycomb Repressive Complex 1 (PRC1)11,13. Both paralogs are essential for PGC development between day 10.5 and 11.5 of gestation. Rnf2 is subsequently required in female PGCs for maintaining high levels of Oct4 and Nanog expression6, and for preventing premature induction of meiotic gene expression and entry into meiotic prophase. Chemical inhibition of RA signaling partially suppresses precocious Oct4 down-regulation and Stra8 activation in Rnf2-deficient female PGCs. Chromatin immunoprecipitation analyses show that Stra8 is a direct target of PRC1 and PRC2 in PGCs. These data demonstrate the importance of PRC1 gene dosage in PGC development and in coordinating the timing of sex differentiation of female PGCs by antagonizing extrinsic RA signaling. Gene expression of mouse primordial germ cells was analysed using Affymetrix microarray. Primodial germ cells were purified from embryos carrying Oct4(deltaPE)-GFP transgene by FACS.

2013-03-14 | E-GEOD-42782 | biostudies-arrayexpress

Early parity-induced gene expression in total mammary epithelial cells in mice

Project description:This study examined the effect of early pregnancy on the gene expression profile of total isolated mammary epithelial cells in mice. Total mammary epithelial cells were isolated from parous and age-matched virgin control mice. Four independent replicates were assessed per treatment group, resulting in a total of 8 samples.

2013-03-17 | E-GEOD-40876 | biostudies-arrayexpress

Early parity-induced gene expression in mouse mammary cell subtypes

Project description:This study examined the effect of early pregnancy on the gene expression profiles of stromal and various epithelial mammary cell subpopulations in mice. Mammary cell subpopulations were isolated from parous and age-matched virgin control mice. Three independent replicates were assessed per cell subpopulation and treatment group, resulting in a total of 35 samples.

2013-03-17 | E-GEOD-40875 | biostudies-arrayexpress

BT474 tumors and MCF10A-HER2/3 cells in the presence or absence of SHP2

Project description:This SuperSeries is composed of the following subset Series: GSE34523: BT474 tumors in the presence or absence of SHP2 GSE34524: MCF10A-HER2/3 cells grown in 3D cultures in the presence or absence of SHP2 Refer to individual Series

2011-12-20 | E-GEOD-34525 | biostudies-arrayexpress

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