PPP1R15B antibody Ab host: Rabbit
- Known as:
- PPP1R15B (anti-) Antibody production species: Rabbit
- Catalog number:
- 'AP55227SU-N
- Product Quantity:
- 0.2 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- PPP1R15B antibody host: Rabbit
Related genes to: PPP1R15B antibody Ab host: Rabbit
- Gene:
- PPP1R15B NIH gene
- Name:
- protein phosphatase 1 regulatory subunit 15B
- Previous symbol:
- -
- Synonyms:
- FLJ14744
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-29
- Date modifiied:
- 2015-11-18
- Gene:
- PPP1R18 NIH gene
- Name:
- protein phosphatase 1 regulatory subunit 18
- Previous symbol:
- KIAA1949
- Synonyms:
- phostensin
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-02
- Date modifiied:
- 2016-10-05
Related products to: PPP1R15B antibody Ab host: Rabbit
Related articles to: PPP1R15B antibody Ab host: Rabbit
- Persistent activation of the integrated stress response (ISR) is a central driver of cognitive decline in both neurodevelopmental and neurodegenerative disorders. However, the cell type-specific mechanisms underlying these deficits remain poorly understood. By integrating single-cell RNA-seq and single-cell assay for transposase-accessible chromatin sequencing, we generated a brain ISR atlas using mice, a clinically relevant model of intellectual disability characterized by selective and persistent ISR activation. We find that distinct brain cell types differentially engage transcriptional and chromatin remodeling programs. Notably, selective deletion of the major ISR downstream effector ATF4 in GABAergic neurons, but not in glutamatergic neurons, exacerbates ISR-mediated cognitive decline in mice, demonstrating that different neuronal subtypes rely on distinct ISR effectors. We define a molecular single-cell signature of persistent ISR activation that serves as a metric of ISR-mediated cellular vulnerability and as a biomarker for cognitive dysfunction across human cognitive disorders. These findings demonstrate that cell type-specific responses drive cognitive dysfunction during persistent ISR activation. - Source: PubMed
Publication date: 2026/07/14
Torkenczy KristofReineke Lucas CDooling Sean WHenderson Benjamin WYang BenjaminHe DongzeMyers Richard MWalter PeterTyanova StefkaCosta-Mattioli Mauro - Chondrodysplasia is a genetic disorder characterized by impaired cartilage development and bone growth. Dysregulation of the endoplasmic reticulum (ER) stress is associated with chondrodysplasia. Here, we demonstrate a critical role for the ER stress regulator PPP1R15B in chondrocyte development. PPP1R15B is a protein phosphatase that constitutively represses eIF2α phosphorylation to attenuate global protein translation in response to stress. Remarkably, deletion of in skeletal progenitors () impairs chondrogenesis, resulting in a disorganized growth plate, reduced trabecular bone, and shortened long bones in mice. Similarly, inducible deletion of in chondroprogenitors () leads to abnormal cartilage development and bone growth. Remarkably, no skeletal phenotype is observed in mice lacking in committed osteoprogenitors () and mature osteoblasts and osteocytes (), indicating that its role is limited to regulation of chondrogenesis, not osteogenic differentiation. Mechanistically, PPP1R15B deletion increases eIF2α phosphorylation, which in turn enhances lipogenic gene expression by suppressing leptin expression. This effect was reversed in mice by reconstitution with wild-type PPP1R15B, but not with a mutant form incapable of eIF2α dephosphorylation. Exogenous expression of leptin also reversed skeletal abnormalities in these mice. Collectively, these findings reveal a critical role for PPP1R15B in cartilage development through its regulation of lipid metabolism. - Source: PubMed
Publication date: 2026/06/01
John Aijaz AhmadYang Yeon-SukXie JunChaugule SachinXu XuLee Ann-HweeLee Kyoung-MiPark Kwang HwanGao GuangpingShim Jae-Hyuck - The integrated stress response (ISR) is essential for cellular homeostasis and cognitive function. We investigated how persistent ISR activation affects cognitive performance by studying the PPP1R15B genetic variant associated with intellectual disability. To model this condition, we generated a mouse line with the pathogenic allele inserted. This variant destabilized the PPP1R15B•PP1 phosphatase complex, causing persistent ISR activation, impaired protein synthesis, and long-term memory deficits. We demonstrated that the cognitive and synaptic impairments in mice arise directly from ISR activation. Furthermore, we characterized DP71L, a viral ortholog of PPP1R15B, which acted as a potent pan-ISR inhibitor. DP71L reversed the cognitive and synaptic deficits across mouse models of Down syndrome, Alzheimer's disease, and aging, and enhanced synaptic plasticity and memory in healthy mice. - Source: PubMed
Publication date: 2026/04/02
Reineke Lucas CZhu Ping JunDalwadi UditDooling Sean WLiu YuweiWang I-ChingYoung-Baird SaraOkoh JamesKuncha Santosh KumarZhou HongyiKannan AksharaPark HyekyungDebeaubien Nicolas ACroll TristanLee D JohnArthur ChristopherDever Thomas EWalter PeterChen JinFrost AdamCosta-Mattioli Mauro - Lenvatinib is a first-line therapy for advanced hepatocellular carcinoma (HCC), yet the emergence of lenvatinib-tolerant persister cells (LTPCs) contributes to therapeutic failure and tumor relapse. The molecular programs that sustain this tolerant state remain insufficiently defined. Here, we investigated the role of the PPP1R15B-ATF4 stress-response axis in mediating lenvatinib tolerance and ferroptosis resistance. - Source: PubMed
Publication date: 2026/01/08
Chen Ming-YaoLai Shiue-WeiCheng Yi-ChiaoYadav Vijesh KumarFong Iat-HangKuo Kuang-TaiLee Kuen-HaurCherng Yih-Giun - Secretory proteins are synthesized in the endoplasmic reticulum (ER) and begin their transport from specialized domains on the ER called ER exit sites (ERES), where COPII proteins assemble. We previously demonstrated that the interaction between TANGO1 and Sec16A is critical for ERES formation. In this study, we reveal that the phosphorylation of TANGO1 and Sec16A is regulated by a FAM83A/CK1α-mediated negative feedback loop. Conversely, their dephosphorylation is regulated in a spatially distinct manner by different phosphatase complexes: PPP6R3/PPP6C for Sec16A and PPP1R15B/PPP1C for TANGO1. Excessive phosphorylation of either TANGO1 or Sec16A leads to ERES disassembly, while excessive dephosphorylation impairs secretion. Our findings demonstrate that maintaining a balanced phosphorylation state of TANGO1 and Sec16A through autoregulation by FAM83A/CK1α and the phosphatases PP1 and PP6 is essential for sustaining proper secretory activity at the ERES. - Source: PubMed
Publication date: 2025/11/25
Maeda MiharuArakawa MasashiWakabayashi MasakiKomatsu YukieSaito Kota