h LIN28 expression Adenovirus
- Known as:
- h LIN28 expression Adenovirus
- Catalog number:
- AVP015
- Product Quantity:
- 1x109 IFU/ml x 200ul
- Category:
- -
- Supplier:
- GenTarget
- Gene target:
- LIN28 expression Adenovirus
Related genes to: h LIN28 expression Adenovirus
- 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
Related articles to: h LIN28 expression Adenovirus
- Precise installation of functional protein domains at endogenous loci is a powerful approach for interrogating protein functions, but its broad application is limited by the low efficiency of homology-directed repair (HDR)-mediated knockin during Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)-Cas9 gene editing. Here, we investigated a simple donor DNA engineering strategy that enhances HDR-mediated gene knockin by appending additional gRNA-recognizable spacer sequences to donor templates. Systematic analysis of linear dsDNA and plasmid donors showed that spacer position, length, and orientation influenced HDR efficiency, and that spacer-containing donors improved knockin across multiple genomic loci, insertion sizes, cell types and delivery modalities. Mechanistic analyses revealed that spacer-containing donors formed stable complexes with Cas9/gRNA and showed increased nuclear localization, supporting nuclear delivery as a key contributor to improved editing outcomes. We then applied this gene-editing strategy to establish a chemical knockdown platform by installing drug-responsive degrons at endogenous loci, generating cell lines in which GSK3β or Lin28A protein could be rapidly, potently and reversibly depleted by drug treatment. These platforms enable selective modulation of endogenous proteins and reveal cellular responses that may differ from those obtained using conventional genetic perturbation. Together, this work establishes a readily implementable framework that integrates improved gene editing with on-demand chemical knockdown of endogenous proteins. - Source: PubMed
Publication date: 2026/09/10
Jang SeeunShin SiyoonJeong YujinAn YubhinHan YeyoungKim HyeonseokLim Donghyun - LIN28A is a conserved RNA-binding protein essential for pluripotency, let-7 miRNA regulation, and cellular metabolism. However, the mechanisms controlling its transcriptional activation during early stem cell fate transitions remain poorly defined. Using the Lin28a locus as a model, we identified multiple intragenic enhancers that generate distinct enhancer RNAs (eRNAs) exhibiting temporally ordered and stimulus-specific activation patterns. Functional perturbation demonstrated that these eRNAs, particularly antisense-derived transcripts, contribute to the regulation of Lin28a transcription and pluripotency maintenance, as their depletion reduced Lin28a expression and impaired embryoid body formation. Distinct environmental inputs induced differential temporal patterns of eRNA activation, accompanied by coordinated changes in enhancer chromatin state and transcription factor occupancy. These findings suggest that intragenic eRNAs make temporally coordinated and differential contributions to stimulus-responsive Lin28a transcriptional dynamics. Together, our findings define a temporally coordinated and context-dependent enhancer logic at the Lin28a locus, in which chromatin state, transcription factor occupancy, and intragenic eRNA induction are integrated to couple external cues with dynamic transcriptional responses during stem cell state transitions. - Source: PubMed
Lee HyohiOh MyunggeunMoon JiinJeong SeunghwaJang YeonjuLee Min HeeUm DahunLee DaeyoupKim Tae-KyungKim Seung-Kyoon - Stem cell based approaches are increasingly studied as models for understanding neurodegenerative diseases. Despite progress, a unified mechanistic understanding of human iPSCs to neural commitment remains incomplete, due to variability in methodologies and experimental conditions, highlighting the need for a more standardized mechanistic framework. This study investigates the transcriptional landscape and regulatory mechanisms underlying the differentiation of induced pluripotent stem cells (iPSCs) towards neural commitment using three orthogonal methodologies across four scRNA seq datasets. In brief, each dataset was processed through a standard Seurat pipeline followed by identification of differentially expressed genes (DEGs) via the Wilcoxon rank-sum test. The significant transcription factors (TFs) were cross validated against the human TF catalogue and ranked accordingly. We identified 15 TFs up-regulated across datasets, and 54 TFs upregulated in three out of four datasets. Among these, ASCL1 emerged as the top candidate. The downregulation of LIN28A and SOX2 is consistent with silencing of the pluripotency network. The second part of the study involved the construction of a co -expression network through a consensus of the four datasets. The network yielded 24 co-expression modules which prioritised hub transcription factors of neural commitment. Module trait correlations were computed with WGCNA, identifying NCAM1 module as top hub. RTN regulon interference and master regulator analysis was applied as a third analysis method. The intersection resulted in identification of LCOR, MEIS3 and EBF1 as the top intramodular hub genes regulators. Current study offers a comprehensive map of key transcriptional dynamics and regulatory nodes involved in iPSC-to-NSC differentiation. This study offers insights into neural development and identifies prioritised candidates for experimental follow-up. - Source: PubMed
Publication date: 2026/07/29
Gupta AyushiSingh Sangeeta - Interspecific hybridisation has been demonstrated to produce offspring that exhibit advantageous traits; however, these offspring frequently exhibit reduced viability or infertility. The cattle-yak, a hybrid animal, is a natural model with which to study hybrid male sterility. The mechanism of male sterility in this species has not yet been fully elucidated. 79.88% of the differentially expressed genes were found to be significantly downregulated during the transition from gonocytes to spermatogonia in the cattle-yak. This resulted in an imbalance of proliferation and differentiation of spermatogonial stem cells in the cattle-yak, leading to a decrease in the number of spermatogonial stem cells. Over-expression of LIN28A has been demonstrated to promote the proliferation of undifferentiated spermatogonia in cattle-yak, primarily by means of up-regulating proliferation-related genes and down-regulating differentiation-related genes. Furthermore, the spermatogenic arrest in the cattle-yak was aggravated at the pachytene primary spermatocyte stage. During this stage, the chromosomes of primary spermatocytes exhibited excessive agglutination and subsequently underwent apoptosis, which ultimately resulted in the atypical configuration of the spermatogenic epithelium of the cattle-yak. The arrest of spermatogenesis in cattle-yak was originated from the transition from gonocytes to spermatogonia, resulting in the destruction of the balance of proliferation and differentiation of spermatogonial stem cells, and aggravated at the primary spermatocyte stage of pachytene, resulting in an absence of sperm in the spermatogenic epithelium. - Source: PubMed
Publication date: 2026/07/31
Zhang PengShen ZhenhuaDong WenjingGuo ShujunMipam TserangDonkoXiong XianrongLi JianCai Xin - Acral melanoma (AM) is a non-ultraviolet (non-UV)-derived subtype of cutaneous melanoma that is associated with worse survival outcomes compared to UV-driven melanomas. AM tumors exhibit distinct molecular characteristics and poor responses to immune checkpoint blockade. Hitherto, the role of transposable elements (TEs), particularly human endogenous retroviruses (HERVs), in AM progression remains incompletely characterized. - Source: PubMed
Publication date: 2026/07/06
Marston Jez LFei TongyiReyes-Gopar HelenaBendall Matthew LNixon Douglas F