ZNF300 antibody - N-terminal region (ARP37793_P050)
- Known as:
- ZNF300 (anti-) - N-terminal region (ARP37793_P050)
- Catalog number:
- arp37793_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNF300 antibody - N-terminal region (ARP37793_P050)
Related genes to: ZNF300 antibody - N-terminal region (ARP37793_P050)
- Gene:
- ZNF300 NIH gene
- Name:
- zinc finger protein 300
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-23
- Date modifiied:
- 2014-11-19
Related products to: ZNF300 antibody - N-terminal region (ARP37793_P050)
Related articles to: ZNF300 antibody - N-terminal region (ARP37793_P050)
- The treatment of metastatic colorectal cancer (mCRC) is impeded by drug resistance. We investigated how prior chemotherapy affects tumor genotype, phenotype, and resistance mechanisms by comparing 35 patient-derived metastatic organoids (PDOs) from pretreated and chemonaive patients with mCRC. Combining PDO drug sensitivity assessments with RNA and whole genome sequencing, we found PDOs from pretreated patients exhibited higher mutational load and more structural variants. Chemotherapy-related mutational signatures correlated with previous exposure. PDOs from oxaliplatin-resistant patients maintained this resistance, showing the upregulation of , , and Hedgehog pathway enrichment. Acquired resistance to 5-FU and irinotecan was only partially captured, with irinotecan resistance linked to specific mutational signatures and deep deletions in common fragile sites, associated with distinct gene expression profiles. Our findings reveal that PDOs capture chemotherapy-induced genomic and phenotypic changes differently depending on the drug, suggesting varied mechanisms of acquired resistance involving both tumor cell-intrinsic properties and dynamic tumor cell states. - Source: PubMed
Publication date: 2025/10/17
Huismans Maarten ASmabers Lidwien PBrunner Sascha Rvan Hoeck ArneKaa Demi van deFranken Ingrid AWensink EmerensKoster JanVolckmann RichardKranenburg OnnoKoopman MiriamSnippert Hugo J GRoodhart Jeanine M L - Genomic imprinting causes parent-of-origin dependent gene expression, primarily driven by a subset of germline differentially methylated regions that function as imprinting control regions at promoter-associated CpG islands. While these mechanisms have been investigated in depth in mice and humans, our understanding of the molecular basis of genomic imprinting in pigs remains limited, particularly at a non-orthologous porcine locus. This study aimed to investigate a pig locus displaying a canonical DNA methylation-dependent imprinting pattern and explore its potential involvement in transcription-coupled imprinting mechanisms. By comparing parthenogenetic and control porcine day-21 embryos, we identified a maternally methylated differentially methylated region in a previously uncharacterized pig locus, LOC100520903 (ZNF300-like), which may serve as an imprinting control region. This was accompanied by a significantly higher paternal mRNA expression of LOC100520903 in control embryos compared to parthenogenetic embryos (p < 0.05), as detected by RNA-seq. At this locus, a previously unannotated transcript with an alternative first exon located far upstream was predominantly expressed in oocytes (supported by >10 RNA-seq junction reads), alongside a promoter marked by H3K4me3 and an adjacent long terminal repeat element (E-value = 5.8e-62). This transcript was no longer detected from embryogenesis onward (0 reads), at which point the annotated LOC100520903 transcripts became expressed. Concurrently, oocyte-specific DNA methylation was observed at the CpG island of the LOC100520903 gene promoter, indicative of maternal methylation. Moreover, in the pig liver and brain, paternal monoallelic expression was consistently observed based on haplotype-tagged RNA-seq reads. Our findings provide mechanistic insights into genomic imprinting at the porcine LOC100520903 locus. - Source: PubMed
Ahn JinsooHwang In-SulPark Mi-RyungHwang SeongsooCho In-CheolLee Kichoon - Fetal sex and placental development impact pregnancy outcomes and fetal-maternal health, but the critical timepoint of placenta establishment in first trimester is understudied in human pregnancies. - Source: PubMed
Publication date: 2024/08/16
Gonzalez Tania LWillson Bryn EWang Erica TTaylor Kent DNovoa AllynsonSwarna AkhilaOrtiz Juanita CZeno Gianna JJefferies Caroline ALawrenson KateRotter Jerome IChen Yii-Der IdaWilliams JohnCui JinruiGoodarzi Mark OPisarska Margareta D - Hepatocellular carcinoma (HCC) is the most common primary malignant tumor of the liver. Currently, the treatments of HCC are limited to surgical resection and liver transplantation, and there is no effective systemic therapy. - Source: PubMed
Publication date: 2024/07/16
Xiang WeiNi JunweiDong LiyangZhu Guoqing - Advancement in genomics technologies have made it possible to identify the genes and their interaction/regulation involved in NSCLC, but the interaction information are scattered over the literature. Thus, there is a need of assembling all the available interaction/regulation information in a single platform which will provide a complete view of NSCLC mechanisms. Further, analysis of the mechanisms underlying NSCLC in humans would benefit substantially from easy access to an electronic network. We, therefore, used manual literature curation and integrated all the existing knowledge of NSCLC biomarkers (mRNA, lncRNA and miRNA) into a single conceptual platform represented through a biological network, termed the LCNetWork which represents 345 genes (195 mRNA, 46 lncRNA and 104 miRNA) and 500 direct interactions that are crucial to the regulation of NSCLC in humans. Furthermore, through exploratory data analysis, we have reported four mRNAs (PLK1, ZNF300, NKX2-1, and EGR1), one lncRNA (UCA1) and five miRNAs (MIR133B, MIR326, MIR429, MIR451A, and MIR944) and MIR193A/UCA1/EGFR axis crucial to NSCLC mechanisms. The GO results suggested their role in post-transcriptional gene silencing and RNA polymerase II activities as causes leading to cancer metastasis. The LCNetWork provides up-to-date knowledge of the genes and their interaction/regulation information in NSCLC and is capable of revealing multiple cancer-gene landscapes. Additionally, the LCNetWork has been provided in the Network Data Exchange portal as an electronic circuit for growth by community-level effort. - Source: PubMed
Publication date: 2022/10/22
Chaturvedi AparnaSom Anup