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Curcumin mitigated aflatoxin B1 induced endoplasmic reticulum stress and gut-kidney axis damage in sheep via regulating the ATF6/GRP78 and IL-1β/NF-κB signaling pathways

ABSTRACT: Curcumin regulated ATF6/GRP78 and IL-1β/NF-κB to alleviate kidney damage

ORGANISM(S): Ovis aries

PROVIDER: GSE309094 | GEO | 2025/09/29

REPOSITORIES: GEO

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Curcumin mitigated aflatoxin B1 induced endoplasmic reticulum stress and gut-kidney axis damage in sheep via regulating the ATF6/GRP78 and IL-1β/NF-κB signaling pathways

Project description:Curcumin mitigated aflatoxin B1 induced endoplasmic reticulum stress and gut-kidney axis damage in sheep via regulating the ATF6/GRP78 and IL-1β/NF-κB signaling pathways

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Targeting CERT sensitizes AML Cells to FLT3 Inhibitors through activating GRP78-ATF6-CHOP Axis

Project description:Ceramide Transfer Protein (CERT) determines the ratio of ceramide and Sphingomyelin in cells. Targeting CERT sensitizes solid cancer cells to chemotherapy. However, the role of CERT in AML remains elusive. Knockdown CERT or its inhibitor HPA-12 inhibited growth and promoted apoptosis in AML cells carrying FLT3-ITD mutation. HPA-12 alone or with the FLT3 inhibitor Crenolanib synergistically inhibited proliferation and triggered apoptosis in FLT3-ITD mutated AML cells in vitro and in vivo. Interestingly, co-treatment of HPA-12 and Crenolanib is effective in FLT3-ITD+ and FLT3-TKD+ AML patients. The synergistic effects were mediated by the endoplasmic reticulum (ER) stress-GRP78/ATF6/CHOP axis and mitophagy. Our data suggest a possible strategy to enhance the efficacy of FLT3 inhibitors in AML.

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Targeting CERT sensitizes AML Cells to FLT3 Inhibitors through activating GRP78-ATF6-CHOP Axis

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Nuclear GRP78 on transcription regulation

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The Unfolded Protein Response Regulator, ATF6, Promotes Mesodermal Differentiation

Project description:ATF6 encodes a transcription factor that is activated during the Unfolded Protein Response to protect cells from ER stress. Loss of ATF6α and its paralog ATF6β, results in embryonic lethality, notochord dysgenesis, and in people, loss of ATF6α specifically, results in malformed neuroretina and congenital vision loss. These phenotypes implicate an essential role for ATF6 during vertebrate development. We investigated the function of ATF6 in development using human stem cells undergoing differentiation into multipotent germ layers, nascent tissues, and organs. We artificially activated ATF6 in stem cells with a recently identified small molecule ATF6 agonist, and we inhibited ATF6 using iPSCs from patients harboring ATF6 mutations. We discovered that ATF6 suppresses pluripotency, enhances differentiation, and surprisingly, guides stem cells toward mesodermal cell fates. Our findings reveal a novel role for ATF6 during differentiation and identify a new strategy to robustly create mesodermal tissues through modulation of the ATF6 arm of the UPR.

2017-11-14 | GSE106847 | GEO

Phosphotyrosine profiling of curcumin-induced signaling

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Multiexon deletion alleles of ATF6 linked to achromatopsia

Project description:Achromatopsia (ACHM) is an autosomal recessive disease that results in severe visual loss. Symptoms of ACHM include impaired visual acuity, nystagmus, and photoaversion starting from infancy; furthermore, ACHM is associated with bilateral foveal hypoplasia and absent or severely reduced cone photoreceptor function on electroretinography. Here, we performed genetic sequencing in 3 patients from 2 families with ACHM, identifying and functionally characterizing 2 mutations in the activating transcription factor 6 (ATF6) gene. We identified a homozygous deletion covering exons 8–14 of the ATF6 gene from 2 siblings from the same family. In another patient from a different family, we identified a heterozygous deletion covering exons 2 and 3 of the ATF6 gene found in trans with a previously identified ATF6 c.970C>T (p.Arg324Cys) ACHM disease allele. Recombinant ATF6 proteins bearing these exon deletions showed markedly impaired transcriptional activity by qPCR and RNA-Seq analysis compared with WT-ATF6. Finally, RNAscope revealed that ATF6 and the related ATF6B transcripts were expressed in cones as well as in all retinal layers in normal human retina. Overall, our data identify loss-of-function ATF6 disease alleles that cause human foveal disease.

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Transcriptomic Profiling of Small Molecule Atf6 Modulators in the Retina

Project description:The Unfolded Protein Response (UPR) maintains endoplasmic reticulum (ER) homeostasis and is essential for retinal health. Activating Transcription Factor 6 (ATF6) controls a key UPR branch and upregulates genes that mitigate ER stress. Small molecule modulators of ATF6 have been characterized in cell culture models that increase or decrease the amount of the cleaved, transcriptional activator domain of ATF6 generated from the full-length precursor. However, the effects of these small molecule ATF6 modulators remains unclear in vivo, in part because of the lack of antibodies that robustly detect the cleaved, activated form of ATF6 in model organisms like mice. Here, we used targeted RNA sequencing (RNA-seq) to assess the transcriptional response to intraocular delivery of Ceapin-A7 (an ATF6 inhibitor) and AA147 (an ATF6 activator) in the mouse retina. Using this strategy, we demonstrate that Ceapin-A7 significantly suppressed ATF6 transcriptional targets, whereas AA147 induced ATF6-regulated genes in retinal tissue of the eye. We also show that neither small molecule ATF6 modulator caused retinal cell death, compromised vision, or triggered ER stress by histology, functional testing, and transcriptional analysis. These results identify a transcriptional strategy to sensitively detect and quantify Ceapin-A7 and AA147 modulation of ATF6 in vivo. These findings also identify non-toxic conditions for further in vivo evaluation of small molecule ATF6 modulators in mouse vision loss disease models linked to ER stress.

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