Ccnyl1 is a newly identified genes, but the founction of which remained unclear, here we used the Ccnyl1 knockout mice to finding clues for its functional roles
CCNYL1, but Not CCNY, Cooperates with CDK16 to Regulate Spermatogenesis in Mouse.
Specimen part
View SamplesInvestigate the effect of jhdm1b on Oct4 mediated reprogramming
The histone demethylases Jhdm1a/1b enhance somatic cell reprogramming in a vitamin-C-dependent manner.
Specimen part, Treatment
View SamplesComparison of transcriptome between control and Tcf1/Lef1-deficient mature CD8 thymocytes Overall design: Control mice or those are deficient for Tcf1 and Lef1 transcription factors (deleted by CD4-Cre) were used to isolate thymocytes. The thymocytes were surface-stained to identify TCRbeta high, CD69–, CD24– CD8+ subsets. These cells were sorted for RNAseq analysis.
Tcf1 and Lef1 transcription factors establish CD8(+) T cell identity through intrinsic HDAC activity.
Specimen part, Subject
View SamplesNasopharyngeal carcinoma is an Epstein-Barr virus-associated epithelial cancer with high prevalence in Southeast Asia. mRNA expression levels were measured for essentially all human genes in nasopharyngeal carcinoma tissue samples and normal nasopharyngeal tissues. Data were analyzed for differential gene expression between tumor and normal tissue.
Upregulated long non-coding RNA AFAP1-AS1 expression is associated with progression and poor prognosis of nasopharyngeal carcinoma.
Disease, Disease stage
View SamplesTwist is a key EMT inducer, expression of Twist will induce EMT in HMLE and breast tumor T47D cells
Disrupting the interaction of BRD4 with diacetylated Twist suppresses tumorigenesis in basal-like breast cancer.
Specimen part, Cell line, Treatment
View SamplesThe human RNA polymerase II-associated factor complex (hPAFc) and its individual subunits have been implicated in human diseases including cancer. However, its involvement in breast cancer cells awaits investigation. Using data mining and human breast cancer tissue microarrays, we found that Ctr9, the key scaffold subunit in hPAFc, is highly expressed in ER+ luminal breast cancer and the high expression of Ctr9 correlates with poor prognosis. Knockdown of Ctr9 in ER+ breast cancer cells almost completely erased estrogen regulated transcriptional response. At the molecular level, Ctr9 enhances ER protein stability, promotes recruitment of ER and RNAPII and stimulates transcription elongation and transcription-coupled histone modifications. Knockdown of Ctr9, but not other hPAFc subunits, alters the morphology, proliferative capacity and tamoxifen-sensitivity of ER+ breast cancer cells. Together, our study reveals that Ctr9, a key subunit of hPAFc, is a central regulator of estrogen signaling that drives ER+ breast tumorigenesis, rendering it a potential target for the treatment of ER+ breast cancer.
Ctr9, a key subunit of PAFc, affects global estrogen signaling and drives ERα-positive breast tumorigenesis.
Specimen part, Cell line
View SamplesHeart formation requires input from two populations of progenitor cells - the first and second heart fields - that differentiate at distinct times and create different cardiac components. The cardiac outflow tract (OFT) is built through recruitment of late-differentiating, second heart field (SHF) -derived cardiomyocytes to the arterial pole of the heart. Mechanisms responsible for selection of an appropriate number of OFT cells from the SHF remain unclear, although several lines of evidence emphasize the importance of FGF signaling in promoting this process. Here, we examine the impact of inhibition of FGF signaling on cardiac transcription profiles in an effort to identify genes operating downstream of FGF during OFT development.
Cadm4 restricts the production of cardiac outflow tract progenitor cells.
Specimen part
View SamplesBasonuclin, which is a zinc-finger protein found in abundance only in the keratinocytes of the stratified epithelium, male germ cells and oocytes, qualifies as a maternal-effect gene because the source of pre-implantation embryonic basonuclin is maternal. Using a transgenic-RNAi approach, we knocked-down basonuclin specifically in mouse oocytes, which led to female sub-fertility. Basonuclin deficiency in oocytes perturbed both RNA polymerase I- and II-mediated transcription and oocyte morphology was affected as evidenced by cytoplasmic and cell surface abnormalities. The affected oocytes, however, could still mature to and arrest at metaphase II and be ovulated, suggesting the impaired pathways were not essential for oocyte development and maturation. Nevertheless, an early embryonic failure in pre-implantation development was identified and likely accounted for the sub-fertility phenotype. These results suggest that basonuclin is a new member of the mammalian maternal-effect genes and interestingly, differs from the previously reported mammalian maternal-effect genes in that it also apparently perturbs oogenesis.
Basonuclin: a novel mammalian maternal-effect gene.
No sample metadata fields
View SamplesThe primary spermatogonial stem cells (SSCs), which arise from gonocytes during neonatal development, serve as a foundational self-renewing reservoir to ensure continuous production of spermatozoa throughout adulthood. The transformation of gonocytes into SSCs takes place in a niche established by Sertoli cells. To date, the factors that guide Sertoli cells to establish the initial stem cell niche remain largely unknown. Using Sertoli cell-specific Arid4b knockout (Arid4bSCKO) mice, we demonstrated that ablation of ARID4B resulted in failure to establish a niche for the SSC formation. We performed RNA-Seq analysis to examine the gene expression profile of the Arid4bSCKO testes in comparison with that of control testes. Overall design: We extracted RNA from testes of the control and Arid4bSCKO mice at postnatal day 1.5 of age. Each genotypic group consisted of three pools of testes, and each pool contained four testes. Purified RNA was processed for RNA-Seq analysis using Illumina HiSeq 2500.
Temporal-Spatial Establishment of Initial Niche for the Primary Spermatogonial Stem Cell Formation Is Determined by an ARID4B Regulatory Network.
Specimen part, Cell line, Subject
View SamplesWe have used RNA-seq to examine RNA differential expression between Procr+ and Procr- vascular endothelial cells in mouse mammary gland Overall design: Examine RNA differential expression among subsets of freshly sorted mouse mammary gland vascular endothelal cells
Identification of blood vascular endothelial stem cells by the expression of protein C receptor.
No sample metadata fields
View Samples