Mouse CST3 _ Cystatin_C _ Cystatin_3 Protein (His Tag)
- Known as:
- Mouse CST3 _ Cystatin_C _ Cystatin_3 Protein (histidine Tag)
- Catalog number:
- 50239-M08H
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- Mouse CST3 _ Cystatin_C Cystatin_3 Protein (His Tag)
Related genes to: Mouse CST3 _ Cystatin_C _ Cystatin_3 Protein (His Tag)
- Gene:
- CST3 NIH gene
- Name:
- cystatin C
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 20p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1990-02-06
- Date modifiied:
- 2016-10-05
- Gene:
- HARS NIH gene
- Name:
- histidyl-tRNA synthetase
- Previous symbol:
- USH3B
- Synonyms:
- HisRS
- Chromosome:
- 5q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
- Gene:
- PVR NIH gene
- Name:
- PVR cell adhesion molecule
- Previous symbol:
- PVS
- Synonyms:
- CD155, HVED, Necl-5, NECL5, Tage4
- Chromosome:
- 19q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-03-14
- Gene:
- TRH-GTG1-1 NIH gene
- Name:
- tRNA-His (anticodon GTG) 1-1
- Previous symbol:
- TRNAH4
- Synonyms:
- tRNA-His-GTG-1-1
- Chromosome:
- 1q21.1
- Locus Type:
- RNA, transfer
- Date approved:
- 2008-08-21
- Date modifiied:
- 2019-04-04
- Gene:
- TRH-GTG1-2 NIH gene
- Name:
- tRNA-His (anticodon GTG) 1-2
- Previous symbol:
- TRNAH10
- Synonyms:
- tRNA-His-GTG-1-2
- Chromosome:
- 1q21.1
- Locus Type:
- RNA, transfer
- Date approved:
- 2008-08-29
- Date modifiied:
- 2019-04-04
Related products to: Mouse CST3 _ Cystatin_C _ Cystatin_3 Protein (His Tag)
Related articles to: Mouse CST3 _ Cystatin_C _ Cystatin_3 Protein (His Tag)
- - Source: PubMed
Publication date: 2024/05/08
Zhang YiWu Zhi-Ying - Composition of the vaginal microbiome in pregnancy is associated with adverse maternal, obstetric, and child health outcomes. Identifying the sources of individual differences in the vaginal microbiome is therefore of considerable clinical and public health interest. The current study tested the hypothesis that vaginal microbiome composition during pregnancy is associated with an individual's experience of affective symptoms and stress exposure. Data were based on a prospective longitudinal study of a diverse and medically healthy community sample of 275 mother-infant pairs. Affective symptoms and stress exposure and select measures of associated biomarkers (diurnal salivary cortisol, serum measures of sex hormones) were collected at each trimester; self-report, clinical, and medical records were used to collect detailed data on socio-demographic factors and health behavior, including diet and sleep. Vaginal microbiome samples were collected in the third trimester (34-40 weeks) and characterized by 16S rRNA sequencing. Identified taxa were clustered into three community state types (CST1-3) based on dissimilarity of vaginal microbiota composition. Results indicate that depressive symptoms during pregnancy were reliably associated with individual taxa and CST3 in the third trimester. Prediction of functional potential from 16S taxonomy revealed a differential abundance of metabolic pathways in CST1-3 and individual taxa, including biosynthetic pathways for the neuroactive metabolites, serotonin and dopamine. With the exception of bioavailable testosterone, no significant associations were found between symptoms- and stress-related biomarkers and CSTs. Our results provide further evidence of how prenatal psychological distress during pregnancy alters the maternal-fetal microbiome ecosystem that may be important for understanding maternal and child health outcomes. - Source: PubMed
Publication date: 2024/04/12
Scheible KristinBeblavy RobertSohn Michael BQui XingGill Ann LNarvaez-Miranda JaniretBrunner JessicaMiller Richard KBarrett Emily SO'Connor Tom GGill Steven R - The decline in muscle strength and function with aging is well recognized, but remains poorly characterized at the molecular level. Here, we report the epigenetic relationship between genome-wide DNA methylation and handgrip strength (HGS) among Chinese monozygotic (MZ) twins. DNA methylation (DNAm) profiling was conducted in whole blood samples through Reduced Representation Bisulfite Sequencing method. Generalized estimating equation was applied to regress the DNAm of each CpG with HGS. The Genomic Regions Enrichment of Annotations Tool was used to perform enrichment analysis. Differentially methylated regions (DMRs) were detected using . Causal inference was performed using Inference about Causation through Examination of Familial Confounding method. Finally, we validated candidate CpGs in community residents. We identified 25 CpGs reaching genome-wide significance level. These CpGs located in 9 genes, especially , , and . Many enriched terms highlighted calcium channels, neuromuscular junctions, and skeletal muscle organ development. We identified 21 DMRs of HGS, with several DMRs within , , , and . Causal inference indicated that the DNAm of 16 top CpGs within , , , , and might influence HGS, while HGS influenced DNAm at two CpGs within and . In validation analysis, methylation levels of six CpGs mapped to and one CpG mapped to were negatively associated with HGS weakness in community population. Our study identified multiple DNAm variants potentially related to HGS, especially CpGs within and . These findings provide new clues to the epigenetic modification underlying muscle strength decline. - Source: PubMed
Publication date: 2024/04/03
Luo JiaWang WeijingLi JingxianDuan HaipingXu ChunshengTian XiaocaoZhang Dongfeng - Post-traumatic epilepsy (PTE) stands as one of the numerous debilitating consequences that follow traumatic brain injury (TBI). Despite its impact on many individuals, the current landscape offers only a limited array of reliable treatment options, and our understanding of the underlying mechanisms and susceptibility factors remains incomplete. Among the potential contributors to epileptogenesis, astrocytes, a type of glial cell, have garnered substantial attention as they are believed to promote hyperexcitability and the development of seizures in the brain following TBI. The current study evaluated the transcriptomic changes in cortical astrocytes derived from animals that developed seizures as a result of severe focal TBI. Using RNA-Seq and ingenuity pathway analysis (IPA), we unveil a distinct gene expression profile in astrocytes, including alterations in genes supporting inflammation, early response modifiers, and neuropeptide-amidating enzymes. The findings underscore the complex molecular dynamics in astrocytes during PTE development, offering insights into therapeutic targets and avenues for further exploration. - Source: PubMed
Publication date: 2024/04/10
Leonard JohnWei XiaoranBrowning JackGudenschwager-Basso Erwin KristobalLi JiangtaoHarris Elizabeth AOlsen Michelle LTheus Michelle H - Cerebral amyloid angiopathy (CAA) is a prevalent vascular dementia and common comorbidity of Alzheimer's disease (AD). While it is known that vascular fibrillar amyloid β (Aβ) deposits leads to vascular deterioration and can drive parenchymal CAA related inflammation (CAA-ri), underlying mechanisms of CAA pathology remain poorly understood. Here, we conducted brain regional proteomic analysis of early and late disease stages in the rTg-DI CAA rat model to gain molecular insight to mechanisms of CAA/CAA-ri progression and identify potential brain protein markers of CAA/CAA-ri. Longitudinal brain regional proteomic analysis revealed increased differentially expressed proteins (DEP) including ANXA3, HTRA1, APOE, CST3, and CLU, shared between the cortex, hippocampus, and thalamus, at both stages of disease in rTg-DI rats. Subsequent pathway analysis indicated pathway enrichment and predicted activation of TGF-β1, which was confirmed by immunolabeling and ELISA. Further, we identified numerous CAA related DEPs associate with astrocytes (HSPB1 and MLC1) and microglia (ANXA3, SPARC, TGF-β1) not previously associated with astrocytes or microglia in other AD models, possibly indicating that they are specific to CAA-ri. Thus, the data presented here identify several potential brain protein biomarkers of CAA/CAA-ri while providing novel molecular and mechanistic insight to mechanisms of CAA and CAA-ri pathological progression and glial cell mediated responses. - Source: PubMed
Publication date: 2024/04/10
Schrader Joseph MXu FengAgostinucci Kevin JDaSilva Nicholas AVan Nostrand William E