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A mouse Embryonic Stem Cell Bank for inducible overexpression of human chromosome 21 genes

ABSTRACT: The HSA21-mES Cell Bank includes, in triplicate clones, thirty-two murine orthologs of HSA21 genes, which can be overexpressed in an inducible manner using the Tet-off system integrated in the Rosa26 locus. The following subset of twenty clones were characterized by microarray analysis: Bach1, Erg, Ets2, Gabpa, ZFP295, Nrip1, Olig1, Olig2, Pknox1, 1810007M14Rik, Runx1, Aire, Sim2, Dscr1, DYRK1A, SNF1LK, Ripk4 , Hunk, Pdxk, Pfkl.

ORGANISM(S): Mus musculus

PROVIDER: GSE19836 | GEO | 2010/12/06

SECONDARY ACCESSION(S): PRJNA122055

REPOSITORIES: GEO

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A mouse Embryonic Stem Cell Bank for inducible overexpression of human chromosome 21 genes

Project description:The HSA21-mES Cell Bank includes, in triplicate clones, thirty-two murine orthologs of HSA21 genes, which can be overexpressed in an inducible manner using the Tet-off system integrated in the Rosa26 locus. The following subset of twenty clones were characterized by microarray analysis: Bach1, Erg, Ets2, Gabpa, ZFP295, Nrip1, Olig1, Olig2, Pknox1, 1810007M14Rik, Runx1, Aire, Sim2, Dscr1, DYRK1A, SNF1LK, Ripk4 , Hunk, Pdxk, Pfkl. Each triplicate clone was transcriptionally profiled by microarray analysis using Affymetrix Mouse 430_2 arrays before and after induction (Affymetrix 430A_2 in case of Runx1), yielding six arrays for each overexpression experiment.

2010-12-06 | E-GEOD-19836 | biostudies-arrayexpress

HSA21 Single-minded 2 (Sim2) binding sites co-localize with super-enhancers and pioneer transcription factors in pluripotent mouse ES cells [ChIP-Seq]

Project description:Down syndrome (DS) results from trisomy of chromosome 21 (HSA21). Some DS phenotypes may be directly or indirectly related to the increased expression of specific HSA21 genes, in particular those encoding transcription factors. The HSA21 encoded Single-minded 2 (SIM2) transcription factor has key neurological functions and is a good candidate to be involved in the cognitive impairment of DS. ChIP-sequencing was used to map SIM2 binding in mouse embryonic stem cells and has revealed 1229 high-confidence SIM2-binding sites. Analysis of the SIM2 target genes confirmed the importance of SIM2 in developmental and neuronal processes and indicated that SIM2 may be a master transcription regulator. Indeed, SIM2 DNA binding sites share sequence specificity and overlapping domains of occupancy with master transcription factors such as SOX2, OCT4, NANOG or KLF4. The association between SIM2 and these pioneer factors is supported by the finding that SIM2 can be co-immunoprecipitated with SOX2, OCT4, NANOG or KLF4. Furthermore, the binding of SIM2 marks a particular sub-category of enhancers known as super-enhancers. These regions are characterized by typical DNA modifications and Mediator co-occupancy (MED1 and MED12). Altogether, we provide evidence that SIM2 binds a specific set of enhancer elements thus explaining how SIM2 can regulate its gene network in DS neuronal features.

2015-06-01 | GSE59378 | GEO

HSA21 Single-minded 2 (Sim2) binding sites co-localize with super-enhancers and pioneer transcription factors in pluripotent mouse ES cells [RNA-Seq]

2015-06-01 | GSE59373 | GEO

Project description:We previously identified a novel SNF1/AMPK-related protein kinase, Hunk, from a mammary tumor arising in an MMTV-neu transgenic mouse. The function of this kinase is unknown. Using targeted deletion in mice, we now demonstrate that Hunk is required for the metastasis of c-myc-induced mammary tumors, but is dispensable for normal development. Reconstitution experiments revealed that Hunk is sufficient to restore the metastatic potential of Hunk-deficient tumor cells, as well as defects in migration and invasion, and does so in a manner that requires its kinase activity. Consistent with a role for Hunk in the progression of human cancers, the human homologue of Hunk is overexpressed in aggressive subsets of carcinomas of the ovary, colon, and breast. In addition, a murine gene expression signature that distinguishes Hunk-wild type from Hunk-deficient mammary tumors predicts clinical outcome in women with breast cancer. Together, these findings establish a role for Hunk in metastasis and an in vivo function for this kinase. Hunk-deficient animals were crossed to mice harboring an MMTV-c-myc transgene (Leder et al., 1986). Hunk heterozygous, MMTV-c-myc mice were backcrossed to Hunk heterozygous animals. MMTV-c-myc female animals of each Hunk genotype were mated twice, then monitored twice weekly for mammary tumors. Mice possessing tumors with a maximum diameter of 20 mm were sacrificed and organs were examined at necropsy. Tumor nodules were identified by examination of organs through a Leica Wild MZ8 dissection microscope.

2009-12-31 | E-GEOD-14226 | biostudies-arrayexpress

2009-12-31 | GSE14226 | GEO

Hunk as aregulator of TNBC genes involve in tumor immunity

Project description:The goal of this study was to target tumor immune specific genes and allowed us to specifically immune profiling what genes are change in HUNK or HUNK knockdown groups. A main objective was to determine if genes related to the citokine signaling pathway were changed in HUNK control compared to HUNK knockdown groups.

2024-06-12 | GSE242859 | GEO

HSL119 results in gene expression changes equivalent to HUNK shRNA

Project description:The goal of this study was to determine the gene similarities and overlap between human HER2+ breast cancer cells treated with a HUNK inhibitor (HSL119) and samples engineered with HUNK shRNA (KD1 and KD2). A main objective was to determine if genes related to the AKT pathway were changed in HUNK treated or HUNK knockdown groups compared to control.

2023-12-05 | GSE233608 | GEO

The involvement of RIPK4 in TNF-α-stimulated IL-6 and IL-8 production by melanoma cells

Project description:The receptor-interacting protein kinase 4 (RIPK4) plays an oncogenic role in melanoma by regulating NFκB and Wnt/β-catenin pathways. As its role in melanoma remains not fully understood, we examined the effects of its downregulation on melanoma transcriptomics. Using RNA-seq, we observed broad transcriptome changes in WM266.4 cells upon RIPK4 downregulation, indicating a complex role for RIPK4 in regulating adhesion, migration, proliferation, and inflammatory processes in melanoma cells. Furthermore, our study highlights the potential functional partners of RIPK4, such as BIRC3, TNF-α receptors, and MAP2K6.

2024-04-27 | GSE263112 | GEO

Hypoxia inhibits HUNK-mediated phosphorylation of GEF-H1 for epithelial-to-mesenchymal transition

Project description:Hypoxia regulates epithelial to mesenchymal transition (EMT) of cancer cells. However, the mechanism underlying hypoxia-mediated EMT remains largely unknow. Here, utilizing colorectal cell carcinoma (CRC) as a model, we find that HUNK inhibits EMT and suppresses metastasis of CRC cells via its substrate GEF-H1 in a kinase-dependent manner. Mechanistically, HUNK directly phosphorylates GEF-H1 at ser645 site, which activates RhoA and consequently leads to a cascade of phosphorylation of LIMK1/CFL-1, thereby stabilizing F-actin and inhibiting EMT. Moreover, hypoxia suppresses HUNK activity and dephosphorylates GEF-H1 to promote EMT. Clinically, the expression levels of both HUNK and phosphorylation of GEH-H1 ser645 are not only downregulated in CRC tissues with metastasis compared to that without metastasis, but also positively correlated among these tissues. Our findings highlight the importance of hypoxia-regulated HUNK kinase activity and phosphorylation of GEF-H1 in regulation of EMT and metastasis of CRC.

2022-05-27 | GSE203440 | GEO

Transcriptional profiles of PA1 teratoma cells transfected by RIPK1, RIPK2, RIPK3, or RIPK4

Project description:RIPK4 but not the related kinases RIPK1, RIPK2, and RIPK3 caused similar transcriptional changes to Wnt3a. PA1 cells were transfected by 8ug RIPK1, RIPK2, RIPK3, or RIPK4 for 48h, RNA were extracted and sequenced.

2013-02-04 | E-GEOD-43362 | biostudies-arrayexpress

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