IMP5{intramembrane protease 5}rabbit.pAb
- Known as:
- IMP5{intramembrane protease 5}host: rabbit.pAb
- Catalog number:
- 201-20-2787
- Product Quantity:
- 0.2ml
- Category:
- -
- Supplier:
- Shanghai Sunred
- Gene target:
- IMP5{intramembrane protease 5}rabbit.pAb
Related genes to: IMP5{intramembrane protease 5}rabbit.pAb
- Gene:
- HTRA1 NIH gene
- Name:
- HtrA serine peptidase 1
- Previous symbol:
- PRSS11
- Synonyms:
- HtrA, IGFBP5-protease, ARMD7
- Chromosome:
- 10q26.13
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-25
- Date modifiied:
- 2016-10-05
Related products to: IMP5{intramembrane protease 5}rabbit.pAb
guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) polyclonal antibody(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,β-cyclohexyl-Ala8,D-Tic16,Arg17,Cys18)-Atrial Natriuretic Factor (6-18) amide (mouse, rabbit, rat)
A71915 98% C69H116N26O15S2 CAS:(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host Rabbit, Extraction-free, CE-marked(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host RabbitExtraction-freeCE-marked(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host: Rabbit, Extraction-free, CE-marked Related articles to: IMP5{intramembrane protease 5}rabbit.pAb
- Cerebral small vessel disease (CSVD) is a major cause of lacunar stroke, vascular cognitive impairment, and gait disturbance, yet the development of disease-modifying therapies is limited by the lack of robust, non-invasive biomarkers of microvascular pathology. Arterial spin labeling (ASL) MRI enables quantitative, non-invasive, contrast-free measurement of cerebral blood flow (CBF) and is well suited for longitudinal studies. In routine clinical and research practice, single-delay three-dimensional pseudo-continuous ASL (pCASL) with an appropriately long post-labeling delay is the workhorse implementation and has already been applied in several CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) and hereditary CSVD cohorts, while more advanced approaches such as multi-delay ASL and diffusion-prepared pCASL can additionally probe arterial transit time (ATT) and blood-brain barrier (BBB) water exchange. CADASIL, caused by pathogenic variants, is a prototypical monogenic CSVD with relatively low etiologic heterogeneity, providing a powerful clinical model in which to study microvascular dysfunction and trial-ready imaging markers. In this review, we synthesize data on ASL in CADASIL, including relationships between CBF, cognition, and lesion burden, evidence from acute encephalopathic episodes, and emerging work on ATT and BBB water exchange. We further compare perfusion profiles across monogenic (-related CSVD, Fabry disease) and sporadic CSVD, and discuss how ASL-derived measures-CBF, ATT, and BBB water exchange rate-can be incorporated as imaging endpoints in CADASIL therapeutic trials. In particular, standardized single-delay three-dimensional pCASL provides a practical, scalable method to quantify regional CBF as a primary perfusion endpoint. - Source: PubMed
Publication date: 2026/04/09
Ihara MasafumiSaito SatoshiFujiwara SatoruTanaka TomotakaAso Toshihiko - Vertebrates grow and mature with age after birth, deteriorate, and eventually die. However, the long lifespan of most vertebrates makes it challenging to identify markers of these distinct stages. Here, we leverage the short-lived vertebrate African Turquoise killifish (N. furzeri) to isolate molecular markers distinguishing gradual aging from late-onset aging. N. furzeri lifespan was divided into four stages-growth/maturation, young, midlife, and old-based on biological parameters. Cellular and molecular changes continually increasing or decreasing with age from young to midlife to old stages were defined as "gradual aging", and changes specifically between midlife and old stages as "late-onset aging". We discovered hepatic lipid droplets formed at birth and disappeared during the midlife stage. Metabolome and gene expression analyses of the liver where the majority of changes occurred identified several metabolites and genes as gradual aging markers (e.g., methylhistidine, glutarylcarnitine, and γ-butyrobetaine) and late-onset aging markers (e.g., creatine, homocitrulline, pipecolic acid, p21, htra1, and slc13a5 genes) providing insights into alternative mechanisms of gradual aging and late-onset aging that may be conserved. Thus, molecular markers reflecting gradual aging and late-onset aging at the organ levels can be isolated using N. furzeri. - Source: PubMed
Publication date: 2026/04/22
Chen JunjieKofuji SatoshiKusaba MizukiAbe KotaSasaki TakehikoIshitani TohruNishina Hiroshi - CARASIL may present without systemic features, and seizures including status epilepticus can occur as late-stage complications. Long-term neurological monitoring is essential even in patients lacking extra-neurological manifestations. - Source: PubMed
Publication date: 2026/04/19
Najafi Mohammad AminAlaei Seyyed AliMajoumerd Alireza AnjamMirghanizadeh Bafghi Seyyed AmirHosseinVajdi MahdiNajafi Mohammad Reza - Ménière's disease (MD), a chronic inflammatory disorder with age-related increased incidence, exhibits poorly understood pathogenesis and limited therapeutic options. Here, we demonstrate that cellular senescence, marked by mitochondrial damage, reactive oxygen species accumulation, and senescence-associated secretory phenotype (SASP), is prevalent in the vestibular tissue of MD patients and an endolymphatic hydrops mouse model. The transcription factor GATA4 is upregulated in MD and mice, and its genetic deletion in hair cells alleviates LPS-induced audio-vestibular dysfunction and cellular senescence in mice and HEI-OC1 cells. Mechanistically, HDAC6 interacts with GATA4 and restrains its nuclear transport, while RNA-seq and ChIP-seq identify HtrA1, a serine protease, as a direct transcriptional target of GATA4. Inhibition of HDAC6 or AAV-mediated HtrA1 overexpression exacerbates MD-like symptoms, whereas inhibition of HtrA1 by Galegenimab ameliorates these phenotypes in mice. In aged mice, GATA4 deletion reduces age-related audio-vestibular deficits and senescence markers. Collectively, our findings establish GATA4 as a critical regulator of cellular senescence and inflammaging in inner ear pathologies, providing promising therapeutic targets for MD and age-related audio-vestibular disorders. - Source: PubMed
Publication date: 2026/04/14
Zhang NaLi NaWang YanZhang JingLiu JiahuiChen LeiSong YongdongMu YurongHan YuechenLyu YafengLi XiaofeiWang HanyueWang JingLu YaoFan ZhaominZhang DaogongWang Haibo - Accurate detection of RNA splice variants is often hindered when transcripts lack large distinguishable exonic regions, making conventional PCR strategies challenging. We developed a simple melting temperature (Tm)-guided exon-exon junction (EEJ) RT-PCR method to enable variant-specific detection under these conditions. Uni-directional primers spanning exon-exon junctions were designed so that approximately each half anneals to adjacent exons. The Tm of each half-site was set >7°C below the annealing temperature, preventing stable binding to individual exons and enforcing junction-dependent amplification. The method was evaluated using HTRA1-AS1 long noncoding RNA variants that share overlapping exon sequences but differ in splice connectivity. HTRA1-AS1 comprises five variants, only one with a large distinguishable exon. Tm-guided EEJ primers robustly discriminated the remaining four variants. After optimization, amplification yielded sharp, single bands with minimal cross-reactivity. Compared with conventional designs, this approach reduced heteroduplex and heteroquadruplex formation, improving band clarity. Sanger sequencing confirmed junction specificity, and the method performed well in multiplex settings. Overall, Tm-guided EEJ RT-PCR is a cost-effective, high-resolution approach for detecting RNA variants lacking easily distinguishable exonic regions, readily compatible with standard RT-PCR and qPCR workflows. - Source: PubMed
Publication date: 2026/04/05
Ahn JunyeopZack Donald JZhang Ping-Wu