FLJ14768 antibody - C-terminal region (ARP30009_T100)
- Known as:
- FLJ14768 (anti-) - C-terminal region (ARP30009_T100)
- Catalog number:
- arp30009_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FLJ14768 antibody - C-terminal region (ARP30009_T100)
Related genes to: FLJ14768 antibody - C-terminal region (ARP30009_T100)
- Gene:
- FIZ1 NIH gene
- Name:
- FLT3 interacting zinc finger 1
- Previous symbol:
- -
- Synonyms:
- FLJ14768, ZNF798
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 2006-08-20
- Date modifiied:
- 2016-02-15
Related products to: FLJ14768 antibody - C-terminal region (ARP30009_T100)
Related articles to: FLJ14768 antibody - C-terminal region (ARP30009_T100)
- Acute kidney injury (AKI) is a serious disease with a high incidence and easy induction. The search for innovative biomarkers and treatment methods is of great significance for improving the prognosis of patients. Autophagy is closely related to the occurrence and development of AKI. This study aims to explore the role of autophagy-related genes (ARGs) as potential biomarkers and therapeutic targets in AKI. - Source: PubMed
Publication date: 2026/02/02
Bai YunqiZhang LiliNie BoSu YixinZhou Jingwei - Testicular differentiation of undifferentiated gonads is triggered by the SRY/Sry (sex-determining region of chromosome Y) gene on the Y chromosome in most mammals. SRY and NR5A1 (nuclear receptor subfamily 5, group A, member 1) proteins regulate transcription of the autosomal SOX9/Sox9 (SRY-box9) gene in XY embryonic gonads, inducing testicular differentiation. One exception, the Amami spiny rat (Tokudaia osimensis), lacks the Y chromosome and Sry. We previously reported that this species has a male-specific duplication upstream of Sox9, and an enhancer (tosEnh14) in the duplication regulates Sox9 transcription without Sry. However, tosEnh14 is not activated by NR5A1 alone, suggesting that another transcription factor(s) which binds to tosEnh14 is necessary. Because this species is endangered and heavily protected, it presents many challenges for genetic studies. Therefore, we explored novel transcription factors that regulate Sox9 via tosEnh14 using mouse samples. To detect proteins that bind to tosEnh14 DNA, Southwestern blotting analysis was performed using mouse embryonic gonad extracts. Bands of a similar molecular weight but prominent in males and faint in females were subjected to mass spectrometry analysis. Peptides derived from 174 genes were identified, and eight genes associated with gene ontology terms such as "DNA binding" and "regulation of transcription by RNA polymerase II" were selected. For further screening, the expression level of each gene was examined using single-cell RNA-sequencing data for mouse progenitor cells, which differentiate into Sertoli cells in mouse embryonic testes and granulosa cells in embryonic ovaries. Finally, five genes (Elf2, Etv6, Fiz1, Gtf2f1 and Trim27) encoding transcription factors, whose expression was confirmed in seminiferous tubules of E13.5 XY embryos by whole-mount in situ hybridization, were selected as candidates. Binding sites for ELF2 and ETV6 are present in the tosEnh14 DNA sequence. Our study contributes to understanding the molecular mechanisms underlying sex determination in mammals. - Source: PubMed
Publication date: 2025/06/05
Mitsukawa ShoichiroMizushima ShuseiKimura YukiKuroiwa Asato - Targeted protein degradation (TPD) has emerged as a powerful strategy to selectively eliminate cellular proteins using small-molecule degraders, offering therapeutic promise for targeting proteins that are otherwise undruggable. However, a remaining challenge is to unambiguously identify primary TPD targets that are distinct from secondary downstream effects in the proteome. Here we introduce an approach for selective analysis of protein degradation by mass spectrometry (DegMS) at proteomic scale, which derives its specificity from the exclusion of confounding effects of altered transcription and translation induced by target depletion. We show that the approach efficiently operates at the timescale of TPD (hours) and we demonstrate its utility by analyzing the cyclin K degraders dCeMM2 and dCeMM4, which induce widespread transcriptional downregulation, and the GSPT1 degrader CC-885, an inhibitor of protein translation. Additionally, we apply DegMS to characterize a previously uncharacterized degrader, and identify the zinc-finger protein FIZ1 as a degraded target. - Source: PubMed
Publication date: 2024/11/12
Jochem MarcoSchrempf AnnaWagner Lina-MarieSegal DmitriCisneros JoseNg AmandaWinter Georg EKrijgsveld Jeroen - Sterile alpha and HEAT/armadillo motif-containing protein (SARM1) was recently described as a NAD-consuming enzyme and has previously been shown to regulate immune responses in macrophages. Neuronal SARM1 is known to contribute to axon degeneration due to its NADase activity. However, how SARM1 affects macrophage metabolism has not been explored. Here, we show that macrophages from Sarm1 mice display elevated NAD concentrations and lower cyclic ADP-ribose, a known product of SARM1-dependent NAD catabolism. Further, SARM1-deficient macrophages showed an increase in the reserve capacity of oxidative phosphorylation and glycolysis compared to WT cells. Stimulation of macrophages to a proinflammatory state by lipopolysaccharide (LPS) revealed that SARM1 restricts the ability of macrophages to upregulate glycolysis and limits the expression of the proinflammatory gene interleukin (Il) 1b, but boosts expression of anti-inflammatory Il10. In contrast, we show macrophages lacking SARM1 induced to an anti-inflammatory state by IL-4 stimulation display increased oxidative phosphorylation and glycolysis, and reduced expression of the anti-inflammatory gene, Fizz1. Overall, these data show that SARM1 fine-tunes immune gene transcription in macrophages via consumption of NAD and altered macrophage metabolism. - Source: PubMed
Publication date: 2024/01/03
Shanahan Katharine ADavis Gavin MDoran Ciara GSugisawa RyoichiDavey Gavin PBowie Andrew G - Identifying the causal interactions in gene-regulatory networks requires an accurate understanding of the time-lagged relationships between transcription factors and their target genes. Here we describe DELAY (short for picting gged Causalit), a convolutional neural network for the inference of gene-regulatory relationships across pseudotime-ordered single-cell trajectories. We show that combining supervised deep learning with joint probability matrices of pseudotime-lagged trajectories allows the network to overcome important limitations of ordinary Granger causality-based methods, for example, the inability to infer cyclic relationships such as feedback loops. Our network outperforms several common methods for inferring gene regulation and, when given partial ground-truth labels, predicts novel regulatory networks from single-cell RNA sequencing (scRNA-seq) and single-cell ATAC sequencing (scATAC-seq) data sets. To validate this approach, we used DELAY to identify important genes and modules in the regulatory network of auditory hair cells, as well as likely DNA-binding partners for two hair cell cofactors (Hist1h1c and Ccnd1) and a novel binding sequence for the hair cell-specific transcription factor Fiz1. We provide an easy-to-use implementation of DELAY under an open-source license at https://github.com/calebclayreagor/DELAY. - Source: PubMed
Publication date: 2023/03/30
Reagor Caleb CVelez-Angel NicolasHudspeth A J