ATP6IP2 _ Renin receptor Antibody
- Known as:
- ATP6IP2 _ Renin receptor Antibody
- Catalog number:
- AF1127a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ATP6IP2 _ Renin receptor Antibody
Related genes to: ATP6IP2 _ Renin receptor Antibody
- Gene:
- ATP6AP2 NIH gene
- Name:
- ATPase H+ transporting accessory protein 2
- Previous symbol:
- ATP6IP2
- Synonyms:
- M8-9, APT6M8-9, ATP6M8-9, PRR, RENR
- Chromosome:
- Xp11.4
- Locus Type:
- gene with protein product
- Date approved:
- 2002-05-23
- Date modifiied:
- 2016-02-11
Related products to: ATP6IP2 _ Renin receptor Antibody
Related articles to: ATP6IP2 _ Renin receptor Antibody
- Each month, the endometrium is shed, regenerated, and transformed in response to changing hormone levels. These processes occur in a tightly regulated manner, and irregularities are linked with reproductive health conditions such as endometriosis and infertility. The renin-angiotensin system is known to be under hormonal control and to drive proliferation and differentiation in tissues, but its expression across the endometrial cycle is not well characterized. Therefore, this study aimed to describe the spatial-temporal localization and gene expression of key initiators of renin-angiotensin system signaling, prorenin, the prorenin receptor, and angiotensinogen, across the endometrial cycle. - Source: PubMed
Publication date: 2026/04/28
Symington Tess LFisher Joshua JZhou WeiDimitriadis EvdokiaLumbers Eugenie RTooney PaulPringle Kirsty G - Granular cell dermatofibroma (GCDF) is a unique histopathological variant of dermatofibroma, characterized by a portion of the lesion composed of cells with abundant granular cytoplasm, resembling granular cell tumors (GCT). GCTs are associated with mutations in V-ATPase component genes; however, the pathogenesis and molecular alterations in GCDF remain uncharacterized. We performed whole exome sequencing on six GCDF cases. Comparative whole exome sequencing analysis of lesional and paired control tissues was conducted to identify genetic mutations in GCDF. Three of the six cases (50%) of GCDF harbored mutations in V-ATPase component genes, including ATP6AP1, ATP6V0C, and ATP6AP2. These findings expand the spectrum of tumors associated with V-ATPase mutations. It is important for dermatopathologists to be aware of clinical, histopathological, and molecular findings in GCDF, and to differentiate these from atypical or malignant GCT, as GCDF are benign and do not need aggressive surgical management. - Source: PubMed
Publication date: 2026/05/11
Jiang XingyuanHu RonghuaChoate Keith APanse Gauri - Patients with Alzheimer's disease (AD) often develop osteoporosis, but the role of bone remodeling in AD remains unclear. We previously showed that osteoblast-specific expression of APP induces bone loss, glial activation, and behavioral deficits, suggesting a bone-to-brain signaling axis. Here, we identify an altered skull bone marrow (SBM)-to-brain axis in AD. Early SBM changes, including reduced cellularity, increased density, and expanded vascular channels to the meninges, occur in multiple APP mouse models. These vascular changes facilitate migration of SBM-derived myeloid cells into the meninges and cortex, improving cerebral blood flow (CBF) and slowing cognitive decline. Notably, these effects are age-dependent, emerging at 6 months but diminishing by 12 months. Enhancing this axis via bone marrow transplantation improves CBF and cognitive function in aged mice, whereas disrupting it through osteoblastic deletion of ATP6AP2 impairs both. Together, these findings reveal a previously unrecognized SBM-to-brain axis that regulates immune, vascular, and cognitive functions, highlighting systemic contributions to AD pathogenesis. - Source: PubMed
Publication date: 2026/05/10
Xiong LeiSun DongGuo Hao-HanLee DaehoonLiu ZhipengMei LinXiong Wen-Cheng - Mycolactone is the virulence toxin of Mycobacterium ulcerans, causative agent of Buruli ulcer. Mycolactone inhibits the Sec61-dependent co-translational translocation of signal peptide-bearing secreted and membrane proteins into the endoplasmic reticulum. Sec61 inhibition leads to accumulation of mislocalised proteins in the cytosol and initially triggers an integrated stress response-dependent activation of autophagy that contributes to cell survival. Here we show sustained exposure to mycolactone blocks late-stage autophagy and induces nuclear translocation of the lysosomal stress marker TFEB. This follows loss of ATP6AP1 and ATP6AP2, Sec61-substrates required for assembly of the Vacuolar-ATPase, leading to reduced lysosomal biogenesis and acidification. These effects are reduced in cells expressing a mycolactone-resistant Sec61α mutant and phenocopied by other Sec61 inhibitors. Loss of lysosomal function compromises the cell's capacity to withstand the proteostatic stress caused by Sec61 inhibition and could impair the ability of phagocytes to combat infection with M. ulcerans and contribute to the tissue necrosis in Buruli ulcer. Furthermore, since Sec61 inhibition is being pursued as a therapeutic target in several diseases, potential drugs should be screened against this activity to avoid unwanted side-effects. - Source: PubMed
Publication date: 2026/04/21
Hall Belinda SOwusu-Boateng KwabenaMcPhail Kerry LShi Wei QSimmonds Rachel E - ATP6AP2 (ATPase H⁺ Transporting Accessory Protein 2) also known as (pro)renin receptor (P)PR is expressed in the central nervous system (CNS). In humans, variants of ATP6AP2 have been linked to neurodegenerative disorders and mental retardation and to changes in the volume of the hippocampus-a limbic brain structure that is capable of adult hippocampal neurogenesis. Cell proliferation in the adult dentate gyrus (DG) can be positively modulated by voluntary exercise. Somewhat surprisingly, we have recently shown that ATP6AP2 overexpression does not show any significant effects on the number of newly generated cells in the DG in transgene-heterozygous mice. Therefore, we now analyzed the effects of voluntary exercise on cell proliferation in the adult hippocampus in female mice overexpressing ATP6AP2 on both alleles. ATP6AP2 mRNA levels in forebrain and hippocampus were increased dose-dependently compared with wild-type mice, with homozygous exhibiting stronger effects than heterozygous mice. Full-length ATP6AP2 protein levels were also increased dose-dependently in forebrain, but the protein fragment representing the soluble prorenin receptor was not. In total hippocampus extracts, no significant differences in ATP6AP2 protein levels were found. However, in the DG, ATP6AP2 immunoreactivity was markedly increased. While the running pattern of mice with access to a running wheel was similar between the groups, cell proliferation, as indicated by BrdU staining, was increased in wild-type mice as expected, but failed to increase in homozygous ATP6AP2 mice. This finding indicates that ATP6AP2 overexpression does not affect basal adult cell proliferation per se but inhibits plastic changes in the rate of cell proliferation. Thus, ATP6AP2 appears to selectively limit exercise-dependent regulation in the hippocampus rather than baseline neurogenic capacity. - Source: PubMed
Publication date: 2026/04/23
Bracke KatharinaKlempin FriederikeWenzel UlrichBader MichaelPeters Jörgvon Bohlen Und Halbach Oliver