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Novus Biologicals
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Santa Cruz Biotechnology
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Novus Biologicals
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Boster Bio
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Babco Inc
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Image Search Results
Journal: Allergology international : official journal of the Japanese Society of Allergology
Article Title: YTHDF1 regulates the proliferation and differentiation of keratinocytes via the PI3K/AKT signaling pathway in atopic dermatitis.
doi: 10.1016/j.alit.2025.04.005
Figure Lengend Snippet: Fig. 7. YTHDF1 regulates the proliferation and differentiation in the DNCB-induced AD mouse model via the PI3K/AKT pathways. (A)The proliferation and differentiation indicators in different groups by WB. (BeC) PCNA and Ki67 protein levels in mice ear tissues by IHC. (DeE) The expression of FLG and LOR by IHC. Original magnification, 200, scale bar ¼ 50 mm. Data were represented as mean ± SEM, n ¼ 6 mice per group. ns, no significance. *P < 0.05, **P < 0.01, and ***P < 0.001. AAV-Ctrl, AAV-GFP control; AAV-YTHDF1; AAV containing YTHDF1.
Article Snippet: Primary antibodies used were as follows: YTHDF1, PCNA, GAPDH,
Techniques: Expressing, Control
Journal: Scientific reports
Article Title: β-endorphin suppresses ultraviolet B irradiation-induced epidermal barrier damage by regulating inflammation-dependent mTORC1 signaling.
doi: 10.1038/s41598-023-49886-5
Figure Lengend Snippet: Figure 2. Treatment with β-endorphin salvaged UVB irradiation-induced increased proliferation and reduced the expression of epidermal differentiation markers in NHKs. (a) Representative images of 5-ethynyl-2ʹ-deoxyuridine (EdU)-positive cells in keratinocytes after UVB irradiation, followed by β-endorphin treatment for 24 h. DAPI: 4′,6-diamidino-2-phenylindole. The histogram shows the quantification of EdU as the percentage of cells with positive staining. (b) NHKs were exposed to 15 mJ/cm2 of UVB light, followed by 100 nM β-endorphin treatment for 48 h. RNA was isolated, and the mRNA expression of loricrin, involucrin, filaggrin, keratin 1, and keratin 10 was analyzed using RT-qPCR. Each mRNA level was normalized to that of the ribosomal gene ribosomal protein L13a (RPL13A). (c) Representative immunoblots showing differentiation markers expression levels. The original blots are presented in Supplementary Fig. S4. The protein expression levels of differentiation markers were determined via western blot analysis, and the quantification of these proteins is shown in the histogram. Data are presented as the mean ± SEM of six independent experiments. # p < 0.05, ##p<0.01, ### p < 0.001 compared to the non-irradiated group, and * p < 0.05, ** p < 0.01, *** p < 0.001 compared to the irradiated vehicle-treated group.
Article Snippet: Proteins were probed with primary antibodies against involucrin (ab68), IκBa (ab32518), phospho-NF-κB (Ser536; ab86299), and NF-κB (ab32536) from Abcam (Cambridge, MA, USA); antibodies against keratin 1 (905204) and keratin 10 (905401) from BioLegend (San Diego, CA, USA); an antibody against filaggrin (PA5-116911) from Invitrogen; an
Techniques: Irradiation, Expressing, Staining, Isolation, Quantitative RT-PCR, Western Blot
Journal: Materials Today Bio
Article Title: Axolotl-derived decellularized skin ECM as a pro-regenerative scaffold for attenuating fibrotic wound healing
doi: 10.1016/j.mtbio.2025.102443
Figure Lengend Snippet: Improved wound healing by A-dECM through restoration of epithelial thickness, skin architecture, and collagen deposition in thermal injury tissues. (A) MT staining of wound tissues captured at 20× magnification. Left: full field view; Right: cropped region from the same image. Both panels share the same scale bar = 100 μm, illustrating collagen deposition and dermal organization. A-dECM-treated tissues exhibited collagen architecture resembling that of normal skin, while M-dECM-treated tissues displayed irregular collagen patterns. (B) Epidermal thickness measurement in wound tissue. (C) Ratio of wound skin thickness relative to adjacent normal tissue. (D) Quantification of collagen density from MT-stained wound sections. (E) Immunohistochemical staining of the epidermal layer at the wound site on day 28 post-injury, showing expression of epithelial differentiation markers K5, K10, and Loricrin. Scale bar = 100 μm. (F) Quantification of layer-specific signal thickness for K5, K10, and Loricrin, expressed as percentage of total epidermal thickness at the wound center (PBS, M-dECM, A-dECM) and in normal skin. Data are presented as mean ± S.D. (n = 6 biologically independent animals per group). Image analysis was performed on 5 randomly selected fields per tissue section. ∗ denote p < 0.05, ∗∗ denotes p < 0.01, ∗∗∗∗ denotes p < 0.0001. Comparisons without statistical annotations were not statistically significant. Statistical analysis was performed using one-way ANOVA followed by post hoc multiple comparisons.
Article Snippet: Sections were then incubated overnight at 4 °C with primary antibodies against CD68 (Abcam, ab125212), iNOS (Thermo Fisher Scientific, PA1-036), CD163 (Abcam, ab182422), K5 (Abcam, ab52635), K10 (Abcam, ab76318), and
Techniques: Staining, Immunohistochemical staining, Expressing
Journal: Human molecular genetics
Article Title: Mutations in SDR9C7 gene encoding an enzyme for vitamin A metabolism underlie autosomal recessive congenital ichthyosis.
doi: 10.1093/hmg/ddw277
Figure Lengend Snippet: Figure 6. Results of indirect-immunofluorescence (IIF) on skin sections. (A-D) We performed double-IIF studies with mouse monoclonal anti-SDR9C7 clone 10B4 (left panels) and rabbit polyclonal anti-loricrin (middle panels) antibodies on paraffin sections of a healthy control individual
Article Snippet: The primary antibodies used were mouse monoclonal anti-SDR9C7 clone 10B4 (diluted 1:100; LifeSpan BioSciences, Inc.), mouse monoclonal anti-SDR9C7 clone 4B5 (diluted 1:150; LifeSpan BioSciences, Inc.),
Techniques: Immunofluorescence, Control
Journal: Frontiers in Cellular Neuroscience
Article Title: Adipose-derived stem cell-conditioned medium mitigates ischemia-induced neuronal injury via the JAK1/STAT3 signaling pathway
doi: 10.3389/fncel.2026.1744887
Figure Lengend Snippet: ADSC-CM promotes nerve fiber regeneration and synaptic plasticity in tMCAO rats through the JAK1/STAT3 signaling pathway. (A) Representative immunofluorescence images of NF-200 (red) in the peri-infarct cortex of each group. (B) Comparison of the NF-200 + nerve fiber density across experimental groups ( n = 4). ( C ) Representative electron micrographs of synaptic ultrastructure in the peri-infarct cortex of each group. The lower panels show magnified views of the areas outlined by red boxes in the respective upper panels. ( D–G ) Comparison of the number of synapses, thickness of PSDs, length of synaptic active zones, and width of synaptic clefts in the peri-infarct cortex across experimental groups ( n = 4). Data are expressed as the means ± SEM. The difference between the groups was assessed using a one-way ANOVA followed by Bonferroni post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bars: 100 μm (A) , 500 nm ( C , upper panel), 100 nm ( C , lower panel).
Article Snippet: Sections were incubated with the following primary antibodies at 4 °C overnight:
Techniques: Immunofluorescence, Comparison