Human Polyclonal ATF6 Ab
- Known as:
- Human Polyclonal ATF6 Antibody
- Catalog number:
- a0202
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal ATF6
Related genes to: Human Polyclonal ATF6 Ab
- Gene:
- ATF6 NIH gene
- Name:
- activating transcription factor 6
- Previous symbol:
- -
- Synonyms:
- ATF6A
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-15
- Date modifiied:
- 2015-09-11
Related products to: Human Polyclonal ATF6 Ab
Related articles to: Human Polyclonal ATF6 Ab
- T-cell acute lymphoblastic leukemia (T-ALL) remains a challenging malignancy with limited targeted therapies. Natural phenanthrene derivatives represent a promising source of antileukemic agents. - Source: PubMed
Publication date: 2026/05/25
Ei Zin ZinNutho BodeeSritularak BoonchooChanvorachote PithiChunhacha Preedakorn - PRKC Apoptosis WT1 Regulator (PAWR) has been implicated in tumorigenesis. However, its role in antiviral innate immunity remains unexplored. Here, we demonstrate that PAWR transcriptionally upregulates RIG-I expression through the transcription factor X-box binding protein 1 (XBP1). Mechanistically, PAWR potentiates the ATF6/IRE1-XBP1 pathway to upregulate spliced form XBP1 (XBP1s) and simultaneously promotes PIM2-mediated phosphorylation of XBP1s at Ser68. Activated XBP1s binds the RIG-I promoter, driving RIG-I expression and amplifying IFN-I responses during RNA virus infection. Most intriguingly, PAWR-silenced THP-1 cells and primary macrophages exhibit attenuated anti-RNA viral IFN-I responses. Pawr-deficient mice are more susceptible to RNA virus challenge. Notably, Arylquin 1, the small molecule activator of PAWR, inhibits VSV replication by boosting the RIG-I-mediated IFN-I response in a PAWR-dependent manner. Collectively, our findings highlight a critical function of PAWR in antiviral innate immunity via the PIM2-XBP1s-RIG-I signaling axis, establishing its potential as a promising therapeutic target for RNA viral infections. - Source: PubMed
Publication date: 2026/06/11
Hou PeiliSun XiaonanZhu HongchaoFeng YueyueLi RuiWang XiaoyunZhang FuzhenWang JunHan YuanyuanHe Daniel ChangWang HongmeiHe Hongbin - Macrophages play a crucial role in the inflammation and wound repair processes of radiation-induced lung injury (RILI). The mechanosensitive ion channel Piezo1 is upregulated during these inflammatory and wound repair processes. However, the involvement of macrophage Piezo1 in the pathogenesis of RILI remains unclear. This study aims to elucidate the regulatory role of Piezo1 in the injury and repair process in RILI and to investigate the underlying mechanisms. - Source: PubMed
Publication date: 2026/06/11
Su WenZhao ZhengtaiZhang HaoLi YayingLiu XinHuang YixinChen AizhuoPang ZhengZhu QingjunLi Jing - Oxaliplatin (OXI), a platinum-based chemotherapeutic agent commonly used in colorectal Cancer treatment, has been linked to significant nephrotoxicity involving apoptosis, endoplasmic reticulum (ER) stress, inflammation, oxidative stress, and autophagy. This study investigated the potential mechanisms involved in kidney damage caused by OXI and explored the renoprotective effects of lycopene (LP) in renal tissues of rats. Biochemical analyses revealed that OXI administration led to elevated serum urea and creatinine levels, increased lipid peroxidation (MDA), and decreased antioxidant defense (SOD, CAT, GPx, GSH), accompanied by suppression of the Nrf-2/HO-1 pathway. Inflammatory markers such as NF-κB, IL-1β, COX-2, TNF-α, and iNOS were significantly upregulated, along with ER stress-related genes (GRP78, ATF6), apoptotic markers (p53, Bax, Bcl-2), and key mediators of autophagy (Beclin-1, JNK). Additionally, Western blot and immunohistochemistry results indicated increased expression of AKT, mTOR, and PI3K proteins in the OXI group, suggesting altered survival signaling. LP treatment ameliorated these pathological alterations by restoring antioxidant enzyme activities, downregulating proinflammatory and proapoptotic signals, mitigating ER stress and autophagy activation, and reducing PI3K/AKT/mTOR protein expression. These findings demonstrate that LP exerts a renoprotective effect against OXI-induced kidney injury through multi-targeted molecular mechanisms, including modulation of inflammation, oxidative stress, autophagy, apoptosis, and survival signaling pathways. - Source: PubMed
Kandemir ÖzgeKüçükler SefaÇomaklı SelimÖzdemir SelçukDalkılınç ElifAydın ŞeymaBayav İbrahimCaglayan CuneytKandemir Fatih Mehmet - Around 70s decade, the discovery of endoplasmic reticulum (ER) chaperones as central regulators of protein folding and quality control set a new paradigm for the understanding of cellular homeostasis. With the arrival of global proteomic approaches, several ER chaperones, including the 78-kDa glucose-regulated protein (GRP78), were unexpectedly found at the cell surface of cancer cells, linking activation of the unfolded protein response (UPR) to tumor biology. Current knowledge suggests that cell surface GRP78 (csGRP78) is a promising therapeutic biomarker, as it is virtually absent on normal cells but enriched on multiple cancers, particularly leukemias. This review summarizes the roles of the three main UPR regulators-IRE1, ATF6, and PERK-and their crosstalk with csGRP78 in leukemia, emphasizing how this network can promote survival or apoptosis. Finally, recent preclinical studies using GRP78-directed CAR-T cells are discussed, highlighting csGRP78 and the UPR pathway as attractive targets for leukemia immunotherapy. - Source: PubMed
Publication date: 2026/06/05
Román-Anguiano Nadia GiovannaGutiérrez-Muñoz Paola AndreaAngeles-Floriano TaniaMartínez-Rodríguez Nancy LuceroGutiérrez-Kobeh LailaJimenez-Martinez Maria CValle-Rios Ricardo