GEO 数据集

主题由标题与摘要自动归类；样本量为数据集标注之和，SuperSeries 可能与其 SubSeries 重复计算。

• RHOX12L counteracts TRIM28-SETDB1 repression to activate embryonic IAP/MERVK retrotransposons [Embryo_Stranded_RNAseq]
  GSE307084Mus musculus样本未标注2026-10-30

  The onset of transcription in pre-implantation embryos includes the widespread transient activation of normally silenced endogenous retroviruses (ERVs) and other retrotransposons. In mice, DUX and OBOX transcription factors activate MERVL, but how other retrotransposons are activated remains largely unknown. Here, we identify RHOX12-like (RHOX12L) as a novel homeodomain-containing factor briefly activated by DUX in 2-cell embryos. Independent of specific DNA-binding activity, RHOX12L counteracts the general ERV repressor SETDB1 to transiently activate thousands of IAP/MERVK loci. Our biochemical studies reveal robust interaction of RHOX12L with SETDB1 as well as CBP/P300 and the BAF complex, concomitant with acetylation and chromatin opening at SETDB1-RHOX12L co-bound sites. In keeping, Rhox12l knockout embryos proved defective in IAP/MERVK activation. Furthermore, RHOX12L downregulates the OCT4 pluripotency network in embryonic stem cells (ESCs), potentially by sequestering OCT4 to de-repressed ERVs bearing upstream OCT4 binding sites. Taken together, we provide a mechanism for the strong, transient activation of the TRIM28/SETDB1-bound retrotransposon repertoire in pre-implantation embryos via co-activator tethering by RHOX12L.
• RHOX12L counteracts TRIM28-SETDB1 repression to activate embryonic IAP/MERVK retrotransposons [ATAC-Seq]
  GSE306939Mus musculus样本未标注2026-10-30

  The onset of transcription in pre-implantation embryos includes the widespread transient activation of normally silenced endogenous retroviruses (ERVs) and other retrotransposons. In mice, DUX and OBOX transcription factors activate MERVL, but how other retrotransposons are activated remains largely unknown. Here, we identify RHOX12-like (RHOX12L) as a novel homeodomain-containing factor briefly activated by DUX in 2-cell embryos. Independent of specific DNA-binding activity, RHOX12L counteracts the general ERV repressor SETDB1 to transiently activate thousands of IAP/MERVK loci. Our biochemical studies reveal robust interaction of RHOX12L with SETDB1 as well as CBP/P300 and the BAF complex, concomitant with acetylation and chromatin opening at SETDB1-RHOX12L co-bound sites. In keeping, Rhox12l knockout embryos proved defective in IAP/MERVK activation. Furthermore, RHOX12L downregulates the OCT4 pluripotency network in embryonic stem cells (ESCs), potentially by sequestering OCT4 to de-repressed ERVs bearing upstream OCT4 binding sites. Taken together, we provide a mechanism for the strong, transient activation of the TRIM28/SETDB1-bound retrotransposon repertoire in pre-implantation embryos via co-activator tethering by RHOX12L.
• RHOX12L counteracts TRIM28-SETDB1 repression to activate embryonic IAP/MERVK retrotransposons [2Cell_full_length_cDNA]
  GSE306936Mus musculus样本未标注2026-10-30

  The onset of transcription in pre-implantation embryos includes the widespread transient activation of normally silenced endogenous retroviruses (ERVs) and other retrotransposons. In mice, DUX and OBOX transcription factors activate MERVL, but how other retrotransposons are activated remains largely unknown. Here, we identify RHOX12-like (RHOX12L) as a novel homeodomain-containing factor briefly activated by DUX in 2-cell embryos. Independent of specific DNA-binding activity, RHOX12L counteracts the general ERV repressor SETDB1 to transiently activate thousands of IAP/MERVK loci. Our biochemical studies reveal robust interaction of RHOX12L with SETDB1 as well as CBP/P300 and the BAF complex, concomitant with acetylation and chromatin opening at SETDB1-RHOX12L co-bound sites. In keeping, Rhox12l knockout embryos proved defective in IAP/MERVK activation. Furthermore, RHOX12L downregulates the OCT4 pluripotency network in embryonic stem cells (ESCs), potentially by sequestering OCT4 to de-repressed ERVs bearing upstream OCT4 binding sites. Taken together, we provide a mechanism for the strong, transient activation of the TRIM28/SETDB1-bound retrotransposon repertoire in pre-implantation embryos via co-activator tethering by RHOX12L.
• RHOX12L counteracts TRIM28-SETDB1 repression to activate embryonic IAP/MERVK retrotransposons [mESC_RNAseq]
  GSE306934Mus musculus样本未标注2026-10-30

  The onset of transcription in pre-implantation embryos includes the widespread transient activation of normally silenced endogenous retroviruses (ERVs) and other retrotransposons. In mice, DUX and OBOX transcription factors activate MERVL, but how other retrotransposons are activated remains largely unknown. Here, we identify RHOX12-like (RHOX12L) as a novel homeodomain-containing factor briefly activated by DUX in 2-cell embryos. Independent of specific DNA-binding activity, RHOX12L counteracts the general ERV repressor SETDB1 to transiently activate thousands of IAP/MERVK loci. Our biochemical studies reveal robust interaction of RHOX12L with SETDB1 as well as CBP/P300 and the BAF complex, concomitant with acetylation and chromatin opening at SETDB1-RHOX12L co-bound sites. In keeping, Rhox12l knockout embryos proved defective in IAP/MERVK activation. Furthermore, RHOX12L downregulates the OCT4 pluripotency network in embryonic stem cells (ESCs), potentially by sequestering OCT4 to de-repressed ERVs bearing upstream OCT4 binding sites. Taken together, we provide a mechanism for the strong, transient activation of the TRIM28/SETDB1-bound retrotransposon repertoire in pre-implantation embryos via co-activator tethering by RHOX12L.
• RHOX12L counteracts TRIM28-SETDB1 repression to activate embryonic IAP/MERVK retrotransposons [KO_embryo_RNAseq]
  GSE306927Mus musculus样本未标注2026-10-30

  The onset of transcription in pre-implantation embryos includes the widespread transient activation of normally silenced endogenous retroviruses (ERVs) and other retrotransposons. In mice, DUX and OBOX transcription factors activate MERVL, but how other retrotransposons are activated remains largely unknown. Here, we identify RHOX12-like (RHOX12L) as a novel homeodomain-containing factor briefly activated by DUX in 2-cell embryos. Independent of specific DNA-binding activity, RHOX12L counteracts the general ERV repressor SETDB1 to transiently activate thousands of IAP/MERVK loci. Our biochemical studies reveal robust interaction of RHOX12L with SETDB1 as well as CBP/P300 and the BAF complex, concomitant with acetylation and chromatin opening at SETDB1-RHOX12L co-bound sites. In keeping, Rhox12l knockout embryos proved defective in IAP/MERVK activation. Furthermore, RHOX12L downregulates the OCT4 pluripotency network in embryonic stem cells (ESCs), potentially by sequestering OCT4 to de-repressed ERVs bearing upstream OCT4 binding sites. Taken together, we provide a mechanism for the strong, transient activation of the TRIM28/SETDB1-bound retrotransposon repertoire in pre-implantation embryos via co-activator tethering by RHOX12L.
• RHOX12L counteracts TRIM28-SETDB1 repression to activate embryonic IAP/MERVK retrotransposons [CUT&Tag]
  GSE306922Mus musculus样本未标注2026-10-30

  The onset of transcription in pre-implantation embryos includes the widespread transient activation of normally silenced endogenous retroviruses (ERVs) and other retrotransposons. In mice, DUX and OBOX transcription factors activate MERVL, but how other retrotransposons are activated remains largely unknown. Here, we identify RHOX12-like (RHOX12L) as a novel homeodomain-containing factor briefly activated by DUX in 2-cell embryos. Independent of specific DNA-binding activity, RHOX12L counteracts the general ERV repressor SETDB1 to transiently activate thousands of IAP/MERVK loci. Our biochemical studies reveal robust interaction of RHOX12L with SETDB1 as well as CBP/P300 and the BAF complex, concomitant with acetylation and chromatin opening at SETDB1-RHOX12L co-bound sites. In keeping, Rhox12l knockout embryos proved defective in IAP/MERVK activation. Furthermore, RHOX12L downregulates the OCT4 pluripotency network in embryonic stem cells (ESCs), potentially by sequestering OCT4 to de-repressed ERVs bearing upstream OCT4 binding sites. Taken together, we provide a mechanism for the strong, transient activation of the TRIM28/SETDB1-bound retrotransposon repertoire in pre-implantation embryos via co-activator tethering by RHOX12L.