Ask about this productRelated genes to: CAPN11 antibody
- Gene:
- CAPN11 NIH gene
- Name:
- calpain 11
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 6p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-19
- Date modifiied:
- 2016-10-05
Related products to: CAPN11 antibody
Related articles to: CAPN11 antibody
- Repressive KRAB domain-containing zinc-finger proteins (KRAB-ZFPs) are abundant in mammalian genomes and contribute both to the silencing of transposable elements (TEs) and to the regulation of developmental stage- and cell type-specific gene expression. Here we describe studies of zinc finger protein 92 (Zfp92), an X-linked KRAB-ZFP that is highly expressed in pancreatic islets of adult mice, by analyzing global Zfp92 knockout (KO) mice. Physiological, transcriptomic and genome-wide chromatin binding studies indicate that the principal function of ZFP92 in mice is to bind to and suppress the activity of B1/Alu type of SINE elements and modulate the activity of surrounding genomic entities. Deletion of Zfp92 leads to changes in expression of select LINE and LTR retroelements and genes located in the vicinity of ZFP92-bound chromatin. The absence of Zfp92 leads to altered expression of specific genes in islets, adipose and muscle that result in modest sex-specific alterations in blood glucose homeostasis, body mass and fat accumulation. In islets, Zfp92 influences blood glucose concentration in postnatal mice via transcriptional effects on Mafb, whereas in adipose and muscle, it regulates Acacb, a rate-limiting enzyme in fatty acid metabolism. In the absence of Zfp92, a novel TE-Capn11 fusion transcript is overexpressed in islets and several other tissues due to de-repression of an IAPez TE adjacent to ZFP92-bound SINE elements in intron 3 of the Capn11 gene. Together, these studies show that ZFP92 functions both to repress specific TEs and to regulate the transcription of specific genes in discrete tissues. - Source: PubMed
Publication date: 2023/05/08
Osipovich Anna BDudek Karrie DTrinh Linh TKim Lily HShrestha ShristiCartailler Jean-PhilippeMagnuson Mark A - Fetal alcohol spectrum disorders (FASDs) are associated with systemic inflammation and neurodevelopmental abnormalities. Several candidate genes were found to be associated with fetal alcohol exposure (FAE)-associated behaviors, but a sex-specific complete transcriptomic analysis was not performed at the adult stage. Recent studies have shown that they are regulated at the developmental stage. However, the sex-specific role of RNA in FAE offspring brain development and function has not been studied yet. Here, we carried out the first systematic RNA profiling by utilizing a high-throughput transcriptomic (RNA-seq) approach in response to FAE in the brain cortex of male and female offspring at adulthood (P60). Our RNA-seq data analysis suggests that the changes in RNA expression in response to FAE are marked sex-specific. We show that the genes Muc3a, Pttg1, Rec8, Clcnka, Capn11, and pnp2 exhibit significantly higher expression in the male offspring than in the female offspring at P60. FAE female mouse brain sequencing data also show an increased expression of Eno1, Tpm3, and Pcdhb2 compared to male offspring. We performed a pathway analysis using a commercial software package (Ingenuity Pathway Analysis). We found that the sex-specific top regulator genes (Rictor, Gaba, Fmri, Mlxipl) are highly associated with eIF2 (translation initiation), synaptogenesis (the formation of synapses between neurons in the nervous system), sirtuin (metabolic regulation), and estrogen receptor (involved in obesity, aging, and cancer) signaling. Taken together, our transcriptomic results demonstrate that FAE differentially alters RNA expression in the adult brain in a sex-specific manner. - Source: PubMed
Publication date: 2023/01/15
Mishra Nitish KShrinath PulastyaRao RadhakrishnaShukla Pradeep K - Obstructive heart defects (OHDs) share common structural lesions in arteries and cardiac valves, accounting for ~25% of all congenital heart defects. OHDs are highly heritable, resulting from interplay among maternal exposures, genetic susceptibilities, and epigenetic phenomena. A genome-wide association study was conducted in National Birth Defects Prevention Study participants (N = 3978; N = 2507), investigating the genetic architecture of OHDs using transmission/disequilibrium tests (TDT) in complete case-parental trios (N = 440; N = 275) and case-control analyses separately in infants (N = 1635; N = 990) and mothers (case status defined by infant; N = 1703; N = 1078). In the TDT analysis, the SLC44A2 single nucleotide polymorphism (SNP) rs2360743 was significantly associated with OHD (p = 4.08 × 10 ; p = 2.44 × 10 ). A CAPN11 SNP (rs55877192) was suggestively associated with OHD (p = 1.61 × 10 ; p = 0.0016). Two other SNPs were suggestively associated (p < 1 × 10 ) with OHD in only the discovery sample. In the case-control analyses, no SNPs were genome-wide significant, and, even with relaxed thresholds ( × < 1 × 10 and p < 0.05), only one SNP (rs188255766) in the infant analysis was associated with OHDs (p = 1.42 × 10 ; p = 0.04). Additional SNPs with p < 1 × 10 were in loci supporting previous findings but did not replicate. Overall, there was modest evidence of an association between rs2360743 and rs55877192 and OHD and some evidence validating previously published findings. - Source: PubMed
Publication date: 2022/04/22
Rashkin Sara RCleves MarioShaw Gary MNembhard Wendy NNestoridi EiriniJenkins Mary MRomitti Paul ALou Xiang-YangBrowne Marilyn LMitchell Laura EOlshan Andrew FLomangino KevinBhattacharyya SudeepaWitte John SHobbs Charlotte A - Neuropathic pain is directly developed from lesions or somatosensory nervous system diseases that are associated with emotion regulation. In general population, the incidence of neuropathic pain ranges from 7% to 10%, but the underlying mechanism remains largely unknown. Neuropathic pain is often associated with structural and functional abnormalities in multiple brain regions, and its regulation has been shown to correspond with the forebrain, including nucleus accumbens (NAc), medial prefrontal cortex (mPFC) and periaqueductal gray (PAG). - Source: PubMed
Li XXu L-SXu Y-FYang QFang Z-XYao MChen W-Y - Firefighting activities appear to increase the risk of acute and chronic lung disease, including malignancy. While self-contained breathing apparatuses (SCBA) mitigate exposures to inhalable asphyxiates and carcinogens, firefighters frequently remove SCBA during overhaul when the firegrounds appear clear of visible smoke. Using a mouse model of overhaul without airway protection, the impact of fireground environment exposure on lung gene expression was assessed to identify transcripts potentially critical to firefighter-related chronic pulmonary illnesses. Lung tissue was collected 2 hrs post-overhaul and evaluated via whole genome transcriptomics by RNA-seq. Although gas metering showed that the fireground overhaul levels of carbon monoxide (CO), carbon dioxide (CO2), hydrogen cyanine (HCN), hydrogen sulfide (H2S) and oxygen (O2) were within NIOSH ceiling recommendations, 3852 lung genes were differentially expressed when mice exposed to overhaul were compared to mice on the fireground but outside the overhaul environment. Importantly, overhaul exposure was associated with an up/down-regulation of 86 genes with a fold change of 1.5 or greater (p<0.5) including the immunomodulatory-linked genes S100a8 and Tnfsf9 (downregulation) and the cancer-linked genes, Capn11 and Rorc (upregulation). Taken together these findings indicate that, without respiratory protection, exposure to the fireground overhaul environment is associated with transcriptional changes impacting proteins potentially related to inflammation-associated lung disease and cancer. - Source: PubMed
Publication date: 2018/08/21
Gainey Stephen JHorn Gavin PTowers Albert EOelschlager Maci LTir Vincent LDrnevich JennyFent Kenneth WKerber StephenSmith Denise LFreund Gregory G