PERK (Phospho-Thr981) Polyclonal Antibody
- Known as:
- PERK (Phospho-Thr981) Polyclonal Antibody
- Catalog number:
- 12379
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- PERK (Phospho-Thr981) Polyclonal Antibody
Related genes to: PERK (Phospho-Thr981) Polyclonal Antibody
- Gene:
- EIF2AK3 NIH gene
- Name:
- eukaryotic translation initiation factor 2 alpha kinase 3
- Previous symbol:
- -
- Synonyms:
- PEK, PERK
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-14
- Date modifiied:
- 2019-04-23
Related products to: PERK (Phospho-Thr981) Polyclonal Antibody
Related articles to: PERK (Phospho-Thr981) Polyclonal Antibody
- Triploid turbot () exhibit superior growth and survival, yet the molecular basis of their sterility-a key trait for aquaculture-remains largely unexplored. This study investigated ovarian development and transcriptomic profiles in diploid and triploid at three key stages (6, 10, and 20 months post-hatch, mph) to elucidate the stage-specific molecular mechanisms underlying triploid sterility. Histological analysis revealed that diploid ovaries progressed through normal oogenesis to the early vitellogenic stage by 20 mph, whereas triploid ovaries were arrested at the oogonial stage, with only occasional primary oocytes and extensive connective tissue infiltration. Comparative transcriptomic analysis identified 13,305, 14,599, and 13,331 differentially expressed genes (DEGs) between triploid and diploid ovaries at 6, 10, and 20 mph, respectively. Functional enrichment analysis showed that DEGs were significantly associated with meiotic processes, cell cycle regulation, energy metabolism, and apoptosis. Key meiotic genes (, , ) were consistently upregulated in triploids across all stages, while the DNA repair gene was paradoxically downregulated, indicating attempted but aberrant meiotic initiation. Oogenesis regulators (, , ) and energy metabolism genes (, , ) were significantly downregulated, whereas apoptosis-related genes (, ) were upregulated. Notably, KEGG pathway analysis revealed stage-specific shifts from stress-induced apoptosis and p53 signaling at early stages to proteasome activation at later stages, suggesting a transition from active germ cell elimination to maintenance of cellular homeostasis in developmentally arrested ovaries. Collectively, these findings demonstrate that triploid sterility is associated with coordinated dysregulation of meiotic progression, metabolic, and apoptotic pathways, providing a high-resolution molecular framework for understanding reproductive failure in triploid fish and informing strategies for optimizing triploid production in aquaculture. - Source: PubMed
Publication date: 2026/04/28
Sun XiaoxuanLi LifangCheng LuyaoMeng ZhenXu WentengLiu Xinfu - Progressive supranuclear palsy (PSP) is a tauopathy and has a multifactorial etiology. The genetic component comprises at least 15 genes with unrelated functions that increase risk for PSP with a high degree of certainty. The function of these genes in increasing risk for PSP is presently unknown. This study was undertaken to identify new pathological pathways of these genes/proteins in increasing risk for PSP. Identification of possible targets and pathways of these genes was investigated using publicly available databases. 13 out of 15 of the risk genes, i.e. , and target microtubules, and directly alter their function via variable mechanisms. We now present data that these pathways are predicted to involve common pathways strongly involving microtubule hemeostasis, such as vesicle transport of misfolded proteins to lysosomes and cellular export. Two genes ( and ) are not obviously directly targeting microtubules. Mutations of the risk genes interfere with microtubular function and/or structure as they relate to axon formation/integrity, axon transport, intracellular organelle transport and communication, and cellular, microtubule - guided waste management. Microtubules may be thought of as a conveyor belt for the distribution of nutrients and waste management. Taken together these alterations include an increased risk of tau precipitation (MAPT) and are molecular drivers of neuronal degeneration in PSP. Although microtubular dysfunction has long been documented in PSP mainly based on the findings related to MAPT, this is the first study of the effect of risk genes in PSP. We demonstrate that most of these genes (13/15) also affect microtubular structure and function. These genes/proteins may also be biased towards neurodegeneration in motor neurons. - Source: PubMed
Publication date: 2026/04/20
Donlon Timothy AMüller Ulrich - Cigarette smoke (CS) is the primary risk factor for the development of chronic obstructive pulmonary disease (COPD). Investigating the impact of CS on human airway epithelium is important for understanding COPD development and combating its effects. While some studies show that long exposure to CS activates inflammasome formation in airway epithelium, leading to cytokines' maturation and release, its acute effect on inflammation regulation requires further elucidation. Due to the importance of acute cellular responses in modulating cell survival and controlling inflammatory outcomes, we examined the effect of acute cigarette smoke extract exposure on human bronchial epithelial cells. Due to the high reactive oxygen species content in CS, we hypothesize that acute CS exposure activates the integrated stress response (ISR) pathway leading to stress granules (SG) formation to facilitate oxidative stress resolution and promote cell survival. Immunostaining, fluorescence confocal imaging, quantitative analyses, and immunoblotting were performed to test our hypothesis. We report here that acute exposure to CS extract triggers canonical SG formation by activating the ISR pathway via the PERK/eIF2α arm in a reactive oxygen species-dependent manner. SG formation is abolished upon inhibiting PERK or eIF2α function, or by scavenging oxidants prior to smoke exposure. Characterizing SG formation in terms of measuring SG size and abundance and the sequestration of the SG marker G3BP1 reveals that SG formation is maximal at 15% CS extract exposure for 2 h and undergoes gradual disassembly at longer exposure times. This is closely dependent on cytoplasmic p-eIF2α levels. These results demonstrate that acute exposure to CS activates the protective ISR pathway to potentially reduce the detrimental effects of CS and promote stress resolution and cell survival. - Source: PubMed
Publication date: 2026/04/21
Bhowmik MousumiZheng ChenkunBekele BisratFailler JessicaKlatt CarlieFarimani SourenJones BryantTyan Chung-ChunAbu-Arish Asmahan - The unfolded protein response (UPR) plays an important role in tumor progression and cellular stress adaptation. In hepatocellular carcinoma (HCC), pharmacological inhibition of the protein kinase R-like endoplasmic reticulum kinase (PERK) is a potential therapeutic strategy, yet its effects on tumor growth and the microenvironment remain unclear. We investigated the selective PERK inhibitor AMG PERK 44 in a diethylnitrosamine (DEN)-induced mouse model of advanced HCC. Tumor burden, proliferation, fibrosis, immune-related gene expression, and ER stress signaling were assessed alongside analyses of single-cell RNA-sequencing data from HCC mouse models and liver-specific PERK knockout mice. Our results show that AMG PERK 44 did not alter tumor number nor cause a decrease in tumor area and proliferation. Furthermore, fibrotic burden was unchanged, although fibrosis architecture and stromal gene expression (TGF-β, CTGF, F4/80) were modified. Despite PERK inhibition, the expression of ER stress associated genes (CHOP, EIF2AK3, ERdj4) increased. Single-cell analysis revealed context-dependent PERK activity, highest in dendritic cells and macrophages under inflammatory and tumor conditions, while PERK knockout livers showed impaired UPR responses after tunicamycin treatment. Finally, AMG PERK 44 did not enhance idarubicin efficacy and caused no major off-target effects. These findings highlight the context-dependent role of PERK in the HCC microenvironment and its implications for targeting UPR pathways in liver cancer. Impact statement This study provides an evaluation of PERK as a therapeutic target in hepatocellular carcinoma by demonstrating that its inhibition does not produce the anticipated anti-tumor effects in advanced disease, but instead exerts nuanced, context-dependent influences on the tumor microenvironment. - Source: PubMed
Publication date: 2026/04/21
Lerma-Clavero AdaKopsida MariaArendt NathalieLennernäs HansSjöblom MarkusHeindryckx Femke - Human leukocyte antigen E (HLA-E) plays a role in tumor immune escape and is associated with poor prognosis in neuroblastoma (NB). This study aimed to investigate the regulatory effect of suberoylanilide hydroxamic acid (SAHA) on HLA-E expression via the PERK/ATF4/CHOP pathway in NB. - Source: PubMed
Publication date: 2026/03/25
Li ZhuoranZhen XiZeng ChenggongMao YanWei ZhiqingZhen Zijun