Rcan1 Antibody - N-terminal region (ARP31631_P050)
- Known as:
- Rcan1 Antibody - N-terminal region (ARP31631_P050)
- Catalog number:
- arp31631_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Rcan1 Antibody - N-terminal region (ARP31631_P050)
Ask about this productRelated genes to: Rcan1 Antibody - N-terminal region (ARP31631_P050)
- Gene:
- RCAN1 NIH gene
- Name:
- regulator of calcineurin 1
- Previous symbol:
- DSCR1
- Synonyms:
- -
- Chromosome:
- 21q22.12
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-09
- Date modifiied:
- 2016-10-05
Related products to: Rcan1 Antibody - N-terminal region (ARP31631_P050)
Related articles to: Rcan1 Antibody - N-terminal region (ARP31631_P050)
- Long-term neuronal plasticity is driven by activity-regulated gene (ARG) expression programs that encode stimulus features in a neuron type-specific manner . ARG programs are typically characterized by rapid induction of immediate early genes (IEGs) without requiring new protein synthesis, followed by induction of secondary response genes regulated by IEG-encoded transcription factors . However, the molecular mechanisms that pattern these programs in specific neuron types in response to physiological stimuli remain unclear. We previously showed that temperature regulates an ARG program in the AFD thermosensory neuron pair to drive behavioral plasticity . Here, by profiling AFD following temperature upshifts of varying durations, we show that ARGs in this neuron exhibit distinct temporal trajectories. Notably, rapidly induced genes do not include known IEGs but are enriched for molecules implicated in signal transduction and navigation. Both rapid and delayed ARG expression require the CMK-1 CaMKI kinase and CRH-1/CREB transcription factor, with CRH-1 acting at both early and late stages. We further define a temporal regulatory cascade in which CREB-dependent induction of the RCAN-1 calcineurin regulator acts in parallel with the MEF-2 transcription factor to repress expression of a delayed ARG at early timepoints. Subsequent downregulation of RCAN-1 likely enables CRH-1-dependent ARG expression at later stages. Our results demonstrate that in addition to classical gene-activating transcriptional cascades, ARG-controlled repressive mechanisms also operate to precisely shape the temporal dynamics of an ARG cascade in a sensory neuron type , and suggest that distinct cell type-specific regulatory pathways may operate across neuron types to drive ARG expression programs. - Source: PubMed
Publication date: 2026/05/16
Bates Samuel GHarris NathanSengupta Piali - Regulator of calcineurin 1 (RCAN1) is an RNA-binding protein with diverse functions, the regulatory mechanisms underlying mitochondrial function in ischemic neuronal injury remain only partially understood. This study identified significantly elevated plasma RCAN1.1 levels in acute ischemic stroke (AIS) patients and demonstrated that mitochondrial translocation of RCAN1.1L within the ischemic penumbra aggravates cerebral infarction by promoting pathological mitochondrial fission and neuronal apoptosis. Mechanistically, in AIS cell and mouse models, multi-omics screening identified activating transcription factor 2 (ATF2) mRNA as a critical downstream target of RCAN1.1L. RCAN1.1L binds to the 2915-2935 nucleotide in the 3'-untranslated region (UTR) of ATF2 mRNA, stabilizing its expression and promoting the accumulation of mitochondrial ATF2 (mtATF2) protein. MtATF2, in turn, binds to and upregulates mitochondrial fission 1 (FIS1) protein, thereby enhancing mitochondrial fission and driving intrinsic apoptosis. Notably, the RNA aptamer R1SR13 competitively binds to RCAN1.1L protein with ATF2 mRNA, exerting neuroprotective effects by disrupting the RCAN1.1L-mtATF2-FIS1 axis. These findings identify RCAN1.1L as an upstream regulator of ATF2 mRNA stability-mediated mitochondrial fission and apoptosis in ischemic penumbra neurons and highlight R1SR13 as a promising therapeutic candidate for preserving neuronal mitochondrial integrity. - Source: PubMed
Publication date: 2026/05/13
Ji YanbinMa XiaochunWang LiyuanLiu FangfeiTang YaoYang XiaxinZhan ZexinLiu ShuangwuZhao JuanWang TanLiu FuchenYu DexinChen YuguoYun YanSun Xiulian - Improving disease resistance in cattle relies on informed breeding and vaccine development, both depend on our understanding of immune mechanisms in cattle. However, transcriptomic studies of bovine immune responses often show considerable variability due to differences in tissue type, pathogen, time point, and experimental design, limiting the generalizability. Meta-analysis integrates multiple transcriptomic studies to identify consistent gene expression patterns and enhance statistical power. We integrated bovine RNA-seq datasets using immune-response specific keywords, species constraints, and high-throughput sequencing filters to prioritize biologically comparable and meta-analysis-ready studies. Specifically, in this study, we performed a meta-analysis of four bovine transcriptomic datasets to identify immune-related differentially expressed genes (DEGs) in Bos taurus. These datasets showed consistent results across analyses and represent immune responses related to mycobacterial infections (Mycobacterium bovis and Mycobacterium avium subsp. paratuberculosis), making them suitable for combined analysis. Our pipeline included FastQC, Trimmomatic, Bowtie2, SAMtools, FeatureCounts, DESeq2, and MetaRNASeq, identifying 28 DEGs (12 upregulated and 16 downregulated). We identified key immune-related genes (IL1A, RGS2, RCAN1, ZBP1, TIMD4, PPARG, TLR10, and ACP5) with known regulatory roles in immunity. KEGG enrichment analysis revealed involvement in necroptosis, osteoclast differentiation, oxytocin signaling, and cGMP-PKG signaling pathways, associated with inflammatory cell death, cytokine signaling, and immune cell differentiation. Using reproducible transcriptomic signals across systematically selected bovine immune datasets rather than relying on single-experiment analyses, we provide a robust meta-analytic framework. This meta-analysis enhances our understanding of conserved immune signaling mechanisms in cattle for identifying conserved immune mechanisms with broader biological and translational relevance. - Source: PubMed
Marimuthu Vennila Kanchana DeviMatheswaran KishoreThambiraja MenakaOnteru Suneel KumarYennamalli Ragothaman M - Calcium ion (Ca) acts as a second messenger involved in various adaptations by activating signaling pathways. The expression of Ca regulators is modified by resistance training. Thus, Ca signaling may be altered during a period of resistance training. In this study, male Sprague-Dawley rats underwent repeated resistance exercise via transcutaneous electromyostimulation, and the expression of Ca-related factors was examined 3 h after the 1st, 5th, and 10th exercise sessions. Expression of sarcolipin (SLN) and regulator of calcineurin 1 (RCAN1) was significantly higher in exercised legs than control legs after the 5th ( < 0.001) and 10th sessions ( < 0.001). Calcineurin expression showed significant main effects of exercise ( = 0.009) and session ( < 0.001). A significant main effect of session was also observed for Ca/calmodulin-dependent protein kinase II (CaMKII) ( < 0.001), CaMKII α ( < 0.046), CaMKII β ( = 0.002), and CaMKII γ ( < 0.001). In contrast, expression of sarcoplasmic reticulum Ca-ATPase (SERCA) did not change with repeated electromyostimulation. Pearson's correlation analysis showed a significant positive correlation between the expression of SLN and RCAN1 ( = 0.630, = 0.005) and between SLN and CaMKII γ ( = 0.471, = 0.048), as well as a trend for a positive correlation between SLN and CaMKII ( = 0.463, = 0.053). These results suggest that repeated sessions of electromyostimulation increase SLN expression, which may in turn contribute to enhanced Ca signaling after exercise. - Source: PubMed
Publication date: 2026/04/21
Okumura KokiTakegaki JunyaSase KoheiFukao NaokiFujita Satoshi - - Source: PubMed
Publication date: 2026/04/27
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