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Oct4 and jhdm1b infected MEF with or without vitamin C treatment

ABSTRACT: Investigate the effect of jhdm1b on Oct4 mediated reprogramming Investigate the effect of vitamin C on the function of jhdm1b

ORGANISM(S): Mus musculus

PROVIDER: GSE32994 | GEO | 2011/11/17

SECONDARY ACCESSION(S): PRJNA146509

REPOSITORIES: GEO

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Oct4 and jhdm1b infected MEF with or without vitamin C treatment

Project description:Investigate the effect of jhdm1b on Oct4 mediated reprogramming Investigate the effect of vitamin C on the function of jhdm1b oct4 and jhdm1b infected MEF with or without vitamin C treatment

2011-11-17 | E-GEOD-32994 | biostudies-arrayexpress

Mus musculus

Project description:Oct4 and jhdm1b infected MEF with or without vitamin C treatment

| PRJNA146509 | ENA

Histone profile for wild type MEF and secondary MEF with Dox-inducible vectors for Klf4, Sox2 and Oct4 (KSO)

Project description:Histone profile for wild type MEF and secondary MEF with Dox-inducible vectors for Klf4, Sox2 and Oct4 (KSO).

2010-12-31 | GSE21271 | GEO

Gene expression analysis during reprogramming with sequential infecion of Oct4/Klf4/cMyc/Sox2

Project description:To further understand the mechanism of reprogramming, the mouse embryonic fibroblast cells were infected with Oct4, Klf4, c-Myc and Sox2 with special sequence. 1) Oct4 and Klf4 containing retrovirus was delivered on day 0. 2) Oct4, Klf4 and c-Myc were delivered on Day 1.5. 3) c-Myc and Sox-2 were deivered on Day 3. 4) Sox2 were delivered on Day 4.5. 5) Vitamin C containging medium were used from Day 6. The gene expression of Day 0 (MEF), Day 1.5, Day 3, Day 4.5 and Day 6 were analyzed with micro array to indentify the possible underlying mechanism. Especially the factors related to MET/EMT, cell cycle and epigenetic were focused. MEF cells were subjected for reprogramming with special protoocl: 1) Oct4 and Klf4 containing retrovirus were delivered on day 0. 2) Oct4, Klf4 and c-Myc were delivered on Day 1.5. 3) c-Myc and Sox-2 were deivered on Day 3. 4) Sox2 were delivered on Day 4.5. 5) Vitamin C containging medium were used from Day 6. RNA on Day 0 (MEF), Day 1.5, Day 3, Day 4.5 and Day 6 were collected for analysis.

2012-07-11 | E-GEOD-39260 | biostudies-arrayexpress

Oct4 re-expression in cervical cancer

Project description:E7 modulates Oct4 re-expression in cervical cancer

2023-04-06 | MSV000091651 | MassIVE

Vitamin D treatment of M.tb. infected macrophages

Project description:As macrophages are the primary site of Mtb infection and are sites of vitamin D signaling, we have used these cells to understand the molecular mechanisms underlying modulation of the immune response by the hormonal form of vitamin D, 1,25-dihydroxyvitamin D (1,25D). Microarrays were used to measure the changes in gene expression induced by 1,25D treatment of H37Rv-infected THP-1 cells

2013-11-28 | GSE52819 | GEO

ChIP Seq of Oct4, Nanog, H3K27me3 in Oct4+/+ and Oct4 +/- mES cells

Project description:ChIP Seq of Oct4, Nanog, H3K27me3 in Oct4+/+ and Oct4 +/- mES cells

| PRJEB1833 | ENA

Histone profile for wild type MEF and secondary MEF with Dox-inducible vectors for Klf4, Sox2 and Oct4 (KSO)

Project description:Histone profile for wild type MEF and secondary MEF with Dox-inducible vectors for Klf4, Sox2 and Oct4 (KSO). ChIP-Seq data for H3K4me3, H3K27me3 and H3K9me3

2010-12-31 | E-GEOD-21271 | biostudies-arrayexpress

Vitamin D treatment of M.tb. infected macrophages

2013-11-28 | E-GEOD-52819 | biostudies-arrayexpress

A balanced Oct4 protein interaction network is crucial for maintaining pluripotency

Project description:Oct4 is considered a master transcription factor for pluripotent cell self-renewal and embryo development. It primarily collaborates with other transcriptional factors or coregulators to maintain pluripotency. However, it is still unclear how Oct4 interacts with its partners. Here, we show that the Oct4 linker interface mediates competing and balanced Oct4 protein interactions which are crucial for maintaining pluripotency. Linker mutant ESCs maintain the key pluripotency genes expression, but show decreased expression of self-renewal genes and increased expression of differentiation genes which result in impaired ESCs self-renewal and early embryonic lethality. Linker mutation dose not affect Oct4 genomic binding and transactivation potential, but breaks the balanced Oct4 interactome. In mutant ESCs, the interaction between Oct4 and Klf5 was decreased, but interactions between Oct4 and Cbx1, Ctr9, Cdc73 were increased which disrupt the epigenetic state of ESCs. Overexpression of Klf5 or knockdown Cbx1, Cdc73 rescue the cellular phenotype of linker mutant ESCs by rebalancing Oct4 interactome indicating that different partners interact with Oct4 competitively. Thus, by showing how Oct4 interacts with different partners, we provide novel molecular insights to explain how Oct4 contributes to the maintenance of pluripotency.

2021-12-10 | PXD017456 | Pride

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