h LIN28 expression Adenovirus, in vivo ready
- Known as:
- h LIN28 expression Adenovirus, vivo ready
- Catalog number:
- AVP015-PBS
- Product Quantity:
- 1x1011 IFU/ml x 50ul
- Category:
- -
- Supplier:
- GenTarget
- Gene target:
- LIN28 expression Adenovirus vivo ready
Related genes to: h LIN28 expression Adenovirus, in vivo ready
- Gene:
- LIN28A NIH gene
- Name:
- lin-28 homolog A
- Previous symbol:
- LIN28
- Synonyms:
- LIN-28, FLJ12457, ZCCHC1, CSDD1
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-21
- Date modifiied:
- 2016-10-05
Related products to: h LIN28 expression Adenovirus, in vivo ready
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- RNA binding protein RBM46, as an integral component of MEIOC-YTHDC2 complex, governs the RNA binding specificity in posttranscriptional regulation of male meiotic initiation. RBM46 is also indispensable for embryonic oocyte development in mice. However, the precise phenotypic consequences and underlying regulatory mechanisms of RBM46 in female germ cells remain largely uncharacterized. Here, we demonstrate that RBM46 deficiency leads to derepression of CCNA2, meiotic arrest at leptotene stage and widespread germ cell apoptosis in embryonic ovaries. Transcriptomic profiling of RBM46-deficient ovaries at embryonic day 16.5 revealed significant upregulation of Stra8 and Lin28a, alongside downregulation of multiple meiotic genes. In HEK293T cells, ectopic co-expression of RBM46, MEIOC and YTHDC2 promoted degradation of reporter mRNAs bearing either Lin28a or Mga 3'UTR. Notably, Deletion of the RBM46-binding motif "AAUCAU" within Lin28a 3'UTR reduced this repressive effect. Collectively, these findings establish an essential role of RBM46 for meiotic initiation in female germ cells and identify Lin28a and Mga transcripts as direct targets subject to RBM46-mediated decay. - Source: PubMed
Publication date: 2026/05/28
Li JiaweiShen JunMa YanqiuZhou Jian - Parkinson's disease (PD) involves selective degeneration of midbrain dopaminergic neurons (mDANs), yet the regulatory networks governing their development remain incompletely understood. ZFHX4 has been linked to neurodevelopment across species and shows reduced expression in the PD midbrain. Through integrative analysis of our multiomic data of mDAN differentiation, we show that ZFHX4 is a super-enhancer-controlled transcription factor induced during mDAN specification. Importantly, ZFHX4 is necessary but not sufficient for mDAN differentiation. Genome-wide profiling of ZFHX4 binding revealed targeting to active promoters, and transcriptomic profiling after ZFHX4 depletion identified primary target genes enriched for cell-cycle regulation. Consistently, ZFHX4-depleted cells showed reduced proliferation and accumulated in G2 phase, impairing cell-cycle progression. LIN28A, an RNA-binding protein involved in stem-cell maintenance and microRNA maturation, is among the strongest upregulated genes upon ZFHX4 depletion, with direct ZFHX4 binding at the locus. Our findings indicate that ZFHX4 regulates mDAN maturation through a mechanism involving the LIN28A-miR-9 axis. - Source: PubMed
Publication date: 2026/05/28
Valceschini ElenaGomez Ramos BorjaOhnmacht JochenGinolhac AurelienCatillon MarieGerard DeborahGaigneaux AnthoulaKyriakis DimitriosGrzyb KamilGlaab EnricoGrünewald AnneSkupin AlexanderSauter ThomasKrüger RejkoSinkkonen Lasse - The transition of embryonic stem cells (ESCs) from a pluripotent state to lineage commitment is governed by complex regulatory mechanisms, including chromatin remodeling, as well as transcriptional and post-transcriptional processes. Recent studies have emphasized the interplay between these mechanisms, revealing intricate, multilayered regulatory networks that require further elucidation. In this study, we reveal a new connection between the RNA-binding protein LIN28A and the epigenetic regulation of ESC differentiation. LIN28A is upregulated during the early stages of neural commitment and undergoes a shift in subcellular localization from the nucleus to the cytoplasm upon differentiation. Generation and analysis of Lin28a knockout (KO) ESCs revealed that, although these cells can self-renew, they exhibit a pronounced defect in differentiating into neural precursors. However, mesodermal and endodermal differentiation proceeds normally in Lin28a KO cells, suggesting a neuronal-specific function for LIN28A. Proteomic analyses revealed a dynamic, context-dependent LIN28A interactome, with distinct sets of putative interacting partners in ESCs compared to those in differentiating cells. Among the ESC-specific putative interactors, we validated an RNA-dependent association of LIN28A with components of Polycomb Repressive Complex 2 (PRC2), a key chromatin-modifying complex that deposits the repressive histone modification H3K27me3. Chromatin immunoprecipitation followed by sequencing (ChIP-seq) demonstrated that loss of LIN28A results in persistent PRC2 occupancy at the promoters of developmental genes, accompanied by partial uncoupling between PRC2 binding and H3K27me3 deposition. Lin28a KO causes differentiation defects that are not rescued by pharmacological inhibition of PRC2 enzymatic activity, suggesting that LIN28A regulates PRC2 chromatin dynamics independently of H3K27me3 deposition. Furthermore, we identified an interaction between LIN28A and the long non-coding RNA Neat1, which may serve as a scaffold facilitating PRC2 eviction from chromatin. Taken together, our findings reveal a previously unrecognized role for LIN28A in regulating PRC2-mediated chromatin dynamics and underscore its importance in epigenetic control of neuronal differentiation. - Source: PubMed
Publication date: 2026/05/05
Piscitelli SilviaCascone EmanuelaD'Ambrosio ChiaraDivisato GiuseppinaGiannino EmiliaDe Lisio LauraLeoni GuidoD'Andrea DanielMatassa Danilo SwannLanzuolo ChiaraRosti ValentinaZizolfi Maria ChiaraMatuozzo Monicadi Patrizio Soldateschi EmanueleMaiuri PaoloScaloni AndreaPassaro FabianaParisi Silvia - The microRNA miR-124 promotes neuronal identity by acting globally, through its multiple targets, at the epigenetic, transcriptional and post-transcriptional levels. We have previously shown that miR-124 acts as a potent driver of the astrocytic fate switch toward an immature neuronal identity, while its supplementation with the neurogenic compound ISX9 enhances in vitro neuronal maturation. Nevertheless, additional cues are needed to enhance the in vivo neurogenic reprogramming capacity of miR-124/ISX9 following neurodegeneration or neurotrauma. In this study, we constructed the core transcriptional regulatory network regulated by miR-124 and ISX9 during astrocyte-to-neuron conversion. Our analysis revealed that the DNA demethylase TET1 is a pivotal transcriptional regulator of the miR-124/ISX9 neurogenic reprogramming process. Silencing of Tet1 impaired the miR-124-mediated neuronal conversion of astrocytes, as well as the ISX9-reinforced differentiation of iNs. We also identified the DNA/RNA binding protein LIN28A as the top mediator of ISX9 neurogenic action and provide evidence that it acts as a coregulator of the expression of synaptic genes, along with TET1. Taken together, our data suggest that TET1 and LIN28A are potent candidates for amplifying miR-124/ISX9 combined in vivo reprogramming action and enhance iNs' differentiation state. - Source: PubMed
Publication date: 2026/04/25
Papadimitriou ElsaIohan Lukas daCCFrazeskou AlexandraXingi EvangeliaCosta Marcos RThomaidou Dimitra - Spermatogonial differentiation is a key step in spermatogenesis, yet the transcriptional programs that control this process are not fully defined. E4f1 has been reported to be essential for embryonic development, mitochondrial function and spermatogonial stem cell (SSC) maintenance in mice. However, its function in spermatogonial differentiation and meiosis progression is unknown. - Source: PubMed
Publication date: 2026/04/14
Wang Fei-ChenHe ZhenYan Rong-GeWang Yu-JunWu Jia-LuYang Qi-En