ARGFX 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- ARGFX 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00503582-T01
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- ARGFX 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: ARGFX 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- ARGFX NIH gene
- Name:
- arginine-fifty homeobox
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-05
- Date modifiied:
- 2015-12-14
Related products to: ARGFX 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: ARGFX 293T Cell Transient Overexpression Lysate(Denatured)
- Somatic cell nuclear transfer (SCNT) is important in assisted reproductive technologies. However, its reprogramming efficiency remains low. A considerable drawback of SCNT-cloned embryos is the reduction in telomerase activity, which is crucial for DNA stability and genetic and epigenetic reprogramming. The present study aimed to examine the effects of madecassic acid (MA), a potent telomerase activator, on the developmental rate, embryonic genome activation, and implantation potential of SCNT-derived bovine embryos. The treatment of bovine signal cell-cloned zygotes with 3.0 μg/mL MA significantly increased embryo cleavage (71.5%) and blastocyst rate (28.1%) compared with that in non-treated (control) SCNT-cloned bovine embryos. In addition, MA treatment enhanced the bovine granulosa cells' telomerase activity and telomerase expression are assessed using qTRAP assay and ELISA. Of note, MA enhanced the expression of embryonic genome activation (EGA)-related genes including , , , , , , and in MA-treated cloned embryos compared to the control group. Moreover, MA-treatment of cloned embryos showed substantially less DNA damage than the control SCNT embryos. Mechanistically, MA activation of telomerase reverse transcriptase (TERT) significantly enhanced the nuclear localization of β-catenin and c-Myc and improved EGA. Reduction in the nuclear localization of this triose may be the leading cause of reduced EGA in cloned embryos. In conclusion, MA impacted the EGA reprogramming and development of cloned bovine embryos via probable activation of TERT. This telomerase activator may have the application of improving SCNT-cloned bovine embryos. - Source: PubMed
Publication date: 2025/07/11
Haider ZaheerUllah SafeerMuhammad TahirPerera Chalani DilshaniKhan Muhammad TayyabJan AsifLee Seung-EunLee Seo-HyunKim Sung WooIdrees MuhammadKong Il-Keun - Understanding the functional regulatory landscape of maternal-to-zygotic transition (MZT) during early human embryo development remains a challenge. In this issue of Developmental Cell, Guo et al. assessed single-cell allele-specific transcriptomics from human preimplantation embryos and identified DPRX and ARGFX genes as pivotal factors whose hampered activation underlies cleavage-stage embryonic arrest. - Source: PubMed
Comar Mehmet-YunusOldak BernardoHanna Jacob H - Cleavage-stage arrest in human embryos substantially limits the success rate of infertility treatment, with maternal-to-zygotic transition (MZT) abnormalities being a potential contributor. However, the underlying mechanisms and regulators remain unclear. Here, by performing allelic transcriptome analysis on human preimplantation embryos, we accurately quantified MZT progression by allelic ratio and identified a fraction of 8-cell embryos, at the appropriate developmental time point and exhibiting normal morphology, were in transcriptionally arrested status. Furthermore, we identified PAIRED (PRD)-like homeobox transcription factors divergent paired-related homeobox (DPRX) and arginine-fifty homeobox (ARGFX) as factors involved in MZT, whose deficiency severely impairs MZT and lineage specification and leads to aberrant retention of histone acetylation. By reversing the acetylation retention caused by DPRX and ARGFX defects, embryonic arrest can be partially rescued. Our study identifies factors involved in human MZT and elucidates the etiology underlying human cleavage-stage arrest. - Source: PubMed
Publication date: 2025/01/13
Guo QianyingXu FanqingSong ShiKong SimingZhai FanXiu YuwenLiu DandanLi MingLian YingDing LingLiu QianYang MingDu ZhengrongWang NanLong ChuanWang XiaomengWang YuqianYan ZhiqiangQiao JieYan LiyingYuan Peng - Embryonic genome activation (EGA) is a critical step in early embryonic development, as it marks the transition from relying on maternal factors to the initiation of transcription from embryo's own genome. The factors associated with EGA are not well understood and need further investigation. PRD-like (PRDL) homeodomain transcription factors (TFs) are considered to play crucial roles in this early event during development but these TFs have evolved differently, even within mammalian lineages. Different numbers of PRDL TFs have been predicted in bovine (Bos taurus); however, their divergent evolution requires species-specific confirmation and functional investigations. - Source: PubMed
Publication date: 2024/11/06
Yaşar BarışBoskovic NinaIvask MarilinWeltner JereJouhilahti Eeva-MariVill PiibeSkoog TiinaJaakma ÜlleKere JuhaBürglin Thomas RKatayama ShintaroOrg TõnisKurg Ants - Early embryonic arrest (EEA) is a critical impediment in assisted reproductive technology (ART), affecting 40% of infertile patients by halting the development of early embryos from the zygote to blastocyst stage, resulting in a lack of viable embryos for successful pregnancy. Despite its prevalence, the molecular mechanism underlying EEA remains elusive. This review synthesizes the latest research on the genetic and molecular factors contributing to EEA, with a focus on maternal, paternal, and embryonic factors. Maternal factors such as irregularities in follicular development and endometrial environment, along with mutations in genes like NLRP5, PADI6, KPNA7, IGF2, and TUBB8, have been implicated in EEA. Specifically, PATL2 mutations are hypothesized to disrupt the maternal-zygotic transition, impairing embryo development. Paternal contributions to EEA are linked to chromosomal variations, epigenetic modifications, and mutations in genes such as CFAP69, ACTL7A, and M1AP, which interfere with sperm development and lead to infertility. Aneuploidy may disrupt spindle assembly checkpoints and pathways including Wnt, MAPK, and Hippo signaling, thereby contributing to EEA. Additionally, key genes involved in embryonic genome activation-such as ZSCAN4, DUXB, DUXA, NANOGNB, DPPA4, GATA6, ARGFX, RBP7, and KLF5-alongside functional disruptions in epigenetic modifications, mitochondrial DNA, and small non-coding RNAs, play critical roles in the onset of EEA. This review provides a comprehensive understanding of the genetic and molecular underpinnings of EEA, offering a theoretical foundation for the diagnosis and potential therapeutic strategies aimed at improving pregnancy outcomes. - Source: PubMed
Publication date: 2024/09/26
Zhang JinyiLv JingQin JulingZhang MingHe XuanyiMa BinyuWan YingjingGao YingWang MeiHong Zhidan