atf6a  (Proteintech)

Journal: iScience

Article Title: Impact of ATF6 deletion on the embryonic brain development

doi: 10.1016/j.isci.2025.112569

Figure Lengend Snippet: Expression of UPR genes in developing brain (A) Expression of UPR genes in wild-type cerebral cortex at different stages of development ( n = 4 brains per time point), data are shown as mean ± SEM. E12.5, E14.5, E16.5, and E18.5 denote embryonic 12.5, 14.5, 16.5, and 18.5 days after gestation, respectively. P0.5 and P56 denote postnatal day 0.5 and 56, respectively. (B) Crossing scheme for parental mating, embryos or neonatal mice were used for experiments after genotyping. (C and D) Expression of Atf6a and Atf6b mRNA (C) ( n = 6–7 brains per group) and protein (D) ( n = 3 brains per group) in E16.5 cerebral cortices from control and dcKO embryos. Data are shown as mean ± SEM. ∗ p < 0.05 and ∗∗∗ p < 0.001 by Mann-Whitney U test. Arrowhead: full length ATF6α and ATF6β, arrow: N-terminal fragment, asterisk: non-specific band.

Article Snippet: Atf6a fl/+ mice and Nes-Cre mice were developed, as previously described, and provided by the Jackson laboratory and by Institute of Resource Development and Analysis, Center for Animal Resources and Development, Kumamoto University, respectively.

Techniques: Expressing, Control, MANN-WHITNEY

Journal: iScience

Article Title: Impact of ATF6 deletion on the embryonic brain development

doi: 10.1016/j.isci.2025.112569

Figure Lengend Snippet: Behavior and brain size of the control and dcKO mice (A) Newborn mice at P0.5 in the same littermate. Arrow indicates a milk spot. (B) Illustration of suckling behavior test. Nipple searching time is shown in the graph as mean ± SEM ( n = 8 for control mice including 4 Atf6a fl/fl Atf6b fl/fl mice and 4 Atf6a fl/fl Atf6b fl/+ mice, n = 5 for dcKO mice). All dcKO mice failed to find and attach to the nipple (arrowhead) after 120 s and were considered negative in this test. (C and D) Neonatal mice after caesarean delivery were monitored in warm-humidified chamber either without feeding ( n = 8 for control mice, n = 3 for dcKO mice, p = 0.5093 by Mantel-Cox test) (C) or with administration of the artificial milk directly into the stomach ( n = 6 for control mice, n = 4 for dcKO mice, p = 0.6822 by Mantel-Cox test). (E) Brains from E16.5 embryos and P0.5 mice. Brain and body weights were measured at both E16.5 ( n = 4–8 embryos for each group) and P0.5 ( n = 9–12 mice for each group). Data are represented as mean ± SEM. ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 by Mann-Whitney U test. Scale bars: 5 mm (A), 2 mm (E).

Article Snippet: Atf6a fl/+ mice and Nes-Cre mice were developed, as previously described, and provided by the Jackson laboratory and by Institute of Resource Development and Analysis, Center for Animal Resources and Development, Kumamoto University, respectively.

Techniques: Control, MANN-WHITNEY

Journal: iScience

Article Title: Impact of ATF6 deletion on the embryonic brain development

doi: 10.1016/j.isci.2025.112569

Figure Lengend Snippet: Impaired neurogenesis and increased cell death in dcKO (A, B, and D) Immunohistochemistry of the brain section from E14.5 control or dcKO embryos for the indicated molecules. Cortical thickness was also measured by the thickness of DAPI positive area (A) ( n = 4–7 brains for each group). Dashed lines indicate brain surface. (C) EdU incorporation was conducted at E14.5 for 1 h to see proliferating cells in S-phase (EdU) (4 control brains including 2 Atf6a fl/fl Atf6b fl/fl embryos and 2 Atf6a fl/fl Atf6b fl/+ embryos, and 4 dcKO brains). (E) Apoptosis was evaluated by TUNEL staining using sections prepared for immunohistochemistry as aforementioned ( n = 4 brains for each group). Dashed lines indicate brain surface and lateral ventricle. Data are represented as mean ± SEM. ∗ p < 0.05 and ∗∗ p < 0.01 by Mann-Whitney U test. Scale bars: 100 μm (A–D), 500 μm (E).

Article Snippet: Atf6a fl/+ mice and Nes-Cre mice were developed, as previously described, and provided by the Jackson laboratory and by Institute of Resource Development and Analysis, Center for Animal Resources and Development, Kumamoto University, respectively.

Techniques: Immunohistochemistry, Control, TUNEL Assay, Staining, MANN-WHITNEY

Journal: iScience

Article Title: Impact of ATF6 deletion on the embryonic brain development

doi: 10.1016/j.isci.2025.112569

Figure Lengend Snippet: Scheme for the roles of ATF6α and ATF6β in the developing brain Deletion of Atf6a and Atf6b genes causes reduced levels of expression of molecular chaperones in the ER, leading to hyperactivation of two other UPR branches and impairment of proteostasis. These changes disrupt the microenvironment in the developing brain, resulting in microcephaly and possibly neonatal death.

Article Snippet: Atf6a fl/+ mice and Nes-Cre mice were developed, as previously described, and provided by the Jackson laboratory and by Institute of Resource Development and Analysis, Center for Animal Resources and Development, Kumamoto University, respectively.

Techniques: Expressing