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rabbit anti human fabp5 primary antibody (Proteintech)

Name: rabbit anti human fabp5 primary antibody
Brand: Proteintech
Rating: 95 (69 reviews)

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Proteintech rabbit anti human fabp5 primary antibody
Rabbit Anti Human Fabp5 Primary Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 69 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 95 stars, based on 69 article reviews

rabbit anti human fabp5 primary antibody - by Bioz Stars, 2026-02

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FABP5 is essential for 2-AG-mediated DSI at CA1 GABA synapses (A) Immunolabelling of FABP5 expression in the hippocampal CA1 region of WT mice. a 1- a 2 , Labeling of FABP5 and the astrocyte marker s100β. a 3 , Triple labeling between the neuronal marker NeuN, FABP5, and s100β. Note the robust colocalization of FABP5 with s100β. Scale bar: 100 μm. a 4 , Higher magnification of NeuN, FABP5 and s100β triple labeling. Scale bar: 10 μm. (B) Lack of FABP5 immunostaining in the hippocampus of FABP5 KO mice. b 1, b 2 , FABP5 and s100β staining. b 3 , Merged image of FABP5, s100β, and DAPI labeling. Scale bar: 100 μm. b 4 , merged image of FABP5, NeuN, and DAPI labeling. Scale bar: 100 μm. (C) Inhibition of FABP5 blunts hippocampal DSI. Left panel illustrates averaged magnitude of DSI obtained in WT ( : 47.41 ± 1.11%; n = 8 cells; N = 3 mice), FABP5 KO ( : 5.26 ± 2.37%; n = 8 cells; N = 3 mice; p = 1.95x10 −11 versus WT), and following FABP5 inhibition with 10 μM SBFI-103 ( : 6.59 ± 2.72%; n = 8 cells; N = 3 mice; p = 3.59x10 −11 versus WT). Upper right panel depicts representative traces of IPSCs recorded before and during DSI. Scale bars: 100 ms, 200 pA. Lower right panel represents the time course of DSI. (D) Deletion of FABP5 does not alter the function of CB1Rs. Upper panel illustrates representative IPSCs traces collected before (1) and during the application of WIN55,212-2 (10 μM) (2) from WT ( ) and KO ( ). Lower panel is a summary of the depression of IPSC amplitude induced by WIN55,212-2 in WT ( : 42.53 ± 6.88%; n = 7 cells; N = 3 mice; p = 1.75x10 −7 versus baseline) and KO ( : 43.01 ± 7.24%; n = 7 cells; N = 3 mice; p = 1.44x10 −7 versus baseline). Scale bars: 50 ms, 50 pA. Data are represented as mean ± SEM. ∗∗∗∗ p < 0.001. one-way ANOVA with Bonferroni’s multiple comparisons test.

Journal: iScience

Article Title: Astrocytic FABP5 mediates retrograde endocannabinoid transport at central synapses

doi: 10.1016/j.isci.2025.112342

Figure Lengend Snippet: FABP5 is essential for 2-AG-mediated DSI at CA1 GABA synapses (A) Immunolabelling of FABP5 expression in the hippocampal CA1 region of WT mice. a 1- a 2 , Labeling of FABP5 and the astrocyte marker s100β. a 3 , Triple labeling between the neuronal marker NeuN, FABP5, and s100β. Note the robust colocalization of FABP5 with s100β. Scale bar: 100 μm. a 4 , Higher magnification of NeuN, FABP5 and s100β triple labeling. Scale bar: 10 μm. (B) Lack of FABP5 immunostaining in the hippocampus of FABP5 KO mice. b 1, b 2 , FABP5 and s100β staining. b 3 , Merged image of FABP5, s100β, and DAPI labeling. Scale bar: 100 μm. b 4 , merged image of FABP5, NeuN, and DAPI labeling. Scale bar: 100 μm. (C) Inhibition of FABP5 blunts hippocampal DSI. Left panel illustrates averaged magnitude of DSI obtained in WT ( : 47.41 ± 1.11%; n = 8 cells; N = 3 mice), FABP5 KO ( : 5.26 ± 2.37%; n = 8 cells; N = 3 mice; p = 1.95x10 −11 versus WT), and following FABP5 inhibition with 10 μM SBFI-103 ( : 6.59 ± 2.72%; n = 8 cells; N = 3 mice; p = 3.59x10 −11 versus WT). Upper right panel depicts representative traces of IPSCs recorded before and during DSI. Scale bars: 100 ms, 200 pA. Lower right panel represents the time course of DSI. (D) Deletion of FABP5 does not alter the function of CB1Rs. Upper panel illustrates representative IPSCs traces collected before (1) and during the application of WIN55,212-2 (10 μM) (2) from WT ( ) and KO ( ). Lower panel is a summary of the depression of IPSC amplitude induced by WIN55,212-2 in WT ( : 42.53 ± 6.88%; n = 7 cells; N = 3 mice; p = 1.75x10 −7 versus baseline) and KO ( : 43.01 ± 7.24%; n = 7 cells; N = 3 mice; p = 1.44x10 −7 versus baseline). Scale bars: 50 ms, 50 pA. Data are represented as mean ± SEM. ∗∗∗∗ p < 0.001. one-way ANOVA with Bonferroni’s multiple comparisons test.

Article Snippet: Hippocampal sections (30 μm) were incubated with the following primary antisera: rabbit anti-FABP5 (BioVendor R&D, RD181060100), goat anti-FABP5 (R&D Systems Inc, #AF1476), mouse anti-NeuN (Millipore, MAB377), rabbit anti-NeuN (Abcam, #AB104225), and mouse anti-s100β (Sigma, #S2532).

Techniques: Expressing, Labeling, Marker, Immunostaining, Staining, Inhibition

Expression of FABP5 in FABP5 KO mice restores hippocampal DSI (A) AAV-mediated expression of FABP5 in astrocytes of the hippocampal CA1 region of FABP5 KO mice. a 1 , Low magnification image of FABP5, DAPI, and s100β labeling. Scale bar: 100 μm. a 2 -a 4 , High magnification labeling of FABP5, s100β, and merge. Scale bar: 10 μm. (B) AAV-mediated expression of FABP5 in neurons of FABP5 KO mice. b 1 , Low magnification labeling of DAPI, NeuN, and FABP5. Scale bar: 100 μm. b 2 -b 4 , High magnification labeling of FABP5, NeuN, and merge with DAPI. Scale bars: 10 μm. (C) Upper image illustrates GFP expression in the CA1 region. Lower image shows recording and stimulating electrodes in the same CA1 region expressing FABP5. (D) Re-expression of FABP5 restores DSI in FABP5 KO mice. D 1 , Averaged magnitude of the DSI in WT ( : 43.18 ± 3.16%; n = 10 cells; N = 3 mice), KO ( : 1.76 ± 0.76%; n = 9 cells; N = 3 mice; p = 5.96x10 −14 versus WT), KO+AAV-CAG-FABP5 ( : 39.63 ± 2.55%; n = 9 cells; N = 3 mice; p = 1 versus WT), and KO+AAV-CAG-EGFP ( : 7.15 ± 1.73%; n = 11 cells; N = 4 mice; p = 2.75x10 −11 versus KO+AAV-CAG-FABP5). D 2 , Summary graph of the time course of the DSI obtained in WT (●), KO ( ), KO+AAV-CAG-FABP5 ( ), and KO+AAV-CAG-EGFP ( ). D 3 , Representative traces of IPSCs recorded before and during DSI from WT ( ), KO ( ), KO+AAV-CAG-FABP5 ( ), and KO+AAV-CAG-EGFP ( ). Scale bars: 50 ms, 200 pA. Data are represented as mean ± SEM. ∗∗∗ p < 0.001, one-way ANOVA, with Bonferroni’s multiple comparisons test.

Journal: iScience

Article Title: Astrocytic FABP5 mediates retrograde endocannabinoid transport at central synapses

doi: 10.1016/j.isci.2025.112342

Figure Lengend Snippet: Expression of FABP5 in FABP5 KO mice restores hippocampal DSI (A) AAV-mediated expression of FABP5 in astrocytes of the hippocampal CA1 region of FABP5 KO mice. a 1 , Low magnification image of FABP5, DAPI, and s100β labeling. Scale bar: 100 μm. a 2 -a 4 , High magnification labeling of FABP5, s100β, and merge. Scale bar: 10 μm. (B) AAV-mediated expression of FABP5 in neurons of FABP5 KO mice. b 1 , Low magnification labeling of DAPI, NeuN, and FABP5. Scale bar: 100 μm. b 2 -b 4 , High magnification labeling of FABP5, NeuN, and merge with DAPI. Scale bars: 10 μm. (C) Upper image illustrates GFP expression in the CA1 region. Lower image shows recording and stimulating electrodes in the same CA1 region expressing FABP5. (D) Re-expression of FABP5 restores DSI in FABP5 KO mice. D 1 , Averaged magnitude of the DSI in WT ( : 43.18 ± 3.16%; n = 10 cells; N = 3 mice), KO ( : 1.76 ± 0.76%; n = 9 cells; N = 3 mice; p = 5.96x10 −14 versus WT), KO+AAV-CAG-FABP5 ( : 39.63 ± 2.55%; n = 9 cells; N = 3 mice; p = 1 versus WT), and KO+AAV-CAG-EGFP ( : 7.15 ± 1.73%; n = 11 cells; N = 4 mice; p = 2.75x10 −11 versus KO+AAV-CAG-FABP5). D 2 , Summary graph of the time course of the DSI obtained in WT (●), KO ( ), KO+AAV-CAG-FABP5 ( ), and KO+AAV-CAG-EGFP ( ). D 3 , Representative traces of IPSCs recorded before and during DSI from WT ( ), KO ( ), KO+AAV-CAG-FABP5 ( ), and KO+AAV-CAG-EGFP ( ). Scale bars: 50 ms, 200 pA. Data are represented as mean ± SEM. ∗∗∗ p < 0.001, one-way ANOVA, with Bonferroni’s multiple comparisons test.

Techniques: Expressing, Labeling

FABP5 MUT fails to rescue hippocampal DSI in FABP5 KO mice (A) Astrocytic expression of FABP5 MUT in the CA1 region of FABP5 KO mice. a 1 , Low magnification image of FABP5, s100β, and DAPI labeling in the CA1 region. Scale bar: 100 μm. a 2 -a 4 , High magnification immunostaining of FABP5 labeling, s100β, and merge. Scale bar: 10 μm. (B) Neuronal expression of FABP5 MUT in the CA1 region of FABP5 KO mice. b 1 , Low magnification image of FABP5, NeuN, and DAPI labeling in the CA1 region. Scale bar: 100 μm. b 2 -b 4 , High magnification immunostaining of FABP5, NeuN, and merge with DAPI. Scale bar: 10 μm. (C) Expression of FABP5 MUT in FABP5 KO mice did not rescue hippocampal DSI. Left panel, summary of time course of DSI recorded from wild-type WT+AAV-CAG-FABP5 MUT ( ), WT+AAV-CAG-EGFP ( ), KO+AAV-CAG-FABP5 MUT ( ), and KO+AAV-CAG-EGFP ( ). Right panel, Sample superimposed IPSC traces collected before and during the DSI. Scale bars: 50 ms, 200 pA (D) Summary of DSI magnitude obtained in WT+AAV-CAG-FABP5 MUT ( : 45.86 ± 5.67%; n = 10 cells; N = 3 mice), WT+AAV-CAG-EGFP ( : 44.28 ± 2.86%; n = 11 cells; N = 3 mice), KO+AAV-CAG-FABP5 MUT ( : 3.19 ± 1.27%; n = 13 cells; N = 3 mice; p = 1.54×10 −11 versus WT+AAV-CAG-FABP5 MUT ), KO+AAV-CAG-EGFP ( : 7.15 ± 1.73%; n = 11 cells; N = 3 mice; p = 1 versus KO+AAV-CAG-FABP5 MUT , p = 1.05×10 −9 versus WT+AAV-CAG-EGFP. (E) Expression of FABP5 MUT in FABP5 KO mice does not affect the depression of IPSC amplitude induced by WIN55,212-2 (10 μM) ( , 34.75 ± 68.28%; n = 7; p = 2.21×10 −4 versus baseline). Inset, Sample IPSCs traces collected before and during the application of WIN55,212-2 (10μM). Scale bars: 25 ms, 50 pA. Data are represented as mean ± SEM. ∗∗∗ p < 0.001, one-way ANOVA with Bonferroni’s multiple comparisons test, or paired sample t-test.

Journal: iScience

Article Title: Astrocytic FABP5 mediates retrograde endocannabinoid transport at central synapses

doi: 10.1016/j.isci.2025.112342

Figure Lengend Snippet: FABP5 MUT fails to rescue hippocampal DSI in FABP5 KO mice (A) Astrocytic expression of FABP5 MUT in the CA1 region of FABP5 KO mice. a 1 , Low magnification image of FABP5, s100β, and DAPI labeling in the CA1 region. Scale bar: 100 μm. a 2 -a 4 , High magnification immunostaining of FABP5 labeling, s100β, and merge. Scale bar: 10 μm. (B) Neuronal expression of FABP5 MUT in the CA1 region of FABP5 KO mice. b 1 , Low magnification image of FABP5, NeuN, and DAPI labeling in the CA1 region. Scale bar: 100 μm. b 2 -b 4 , High magnification immunostaining of FABP5, NeuN, and merge with DAPI. Scale bar: 10 μm. (C) Expression of FABP5 MUT in FABP5 KO mice did not rescue hippocampal DSI. Left panel, summary of time course of DSI recorded from wild-type WT+AAV-CAG-FABP5 MUT ( ), WT+AAV-CAG-EGFP ( ), KO+AAV-CAG-FABP5 MUT ( ), and KO+AAV-CAG-EGFP ( ). Right panel, Sample superimposed IPSC traces collected before and during the DSI. Scale bars: 50 ms, 200 pA (D) Summary of DSI magnitude obtained in WT+AAV-CAG-FABP5 MUT ( : 45.86 ± 5.67%; n = 10 cells; N = 3 mice), WT+AAV-CAG-EGFP ( : 44.28 ± 2.86%; n = 11 cells; N = 3 mice), KO+AAV-CAG-FABP5 MUT ( : 3.19 ± 1.27%; n = 13 cells; N = 3 mice; p = 1.54×10 −11 versus WT+AAV-CAG-FABP5 MUT ), KO+AAV-CAG-EGFP ( : 7.15 ± 1.73%; n = 11 cells; N = 3 mice; p = 1 versus KO+AAV-CAG-FABP5 MUT , p = 1.05×10 −9 versus WT+AAV-CAG-EGFP. (E) Expression of FABP5 MUT in FABP5 KO mice does not affect the depression of IPSC amplitude induced by WIN55,212-2 (10 μM) ( , 34.75 ± 68.28%; n = 7; p = 2.21×10 −4 versus baseline). Inset, Sample IPSCs traces collected before and during the application of WIN55,212-2 (10μM). Scale bars: 25 ms, 50 pA. Data are represented as mean ± SEM. ∗∗∗ p < 0.001, one-way ANOVA with Bonferroni’s multiple comparisons test, or paired sample t-test.

Techniques: Expressing, Labeling, Immunostaining

Extracellular pool of FABP5 mediates hippocampal DSI (A) Secreted FABP5 variant (FABP5 SEC ) binds to 2-AG with comparable affinity to WT FABP5 (FABP5 Ki: 1.0 ± 0.1 μM; FABP5 SEC Ki: 1.6 ± 0.2 μM, n = 4). (B) AAV-mediated expression of FABP5 SEC in CA1 astrocytes of FABP5 KO mice. b 1 -b 3 , Immunolabelling for FABP5, s100β, and merge with DAPI. Scale bar: 10 μm. (C) Neuronal expression of FABP5 SEC in the CA1 region. c 1 -c 3 , Immunolabelling for FABP5, NeuN, and merge with DAPI. Scale bar: 10 μm. (D) Expression of FABP5 SEC but not FABP7 restores DSI in FABP5 KO mice. D 1 , left panel, Summary of the time course of hippocampal DSI recorded from WT ( ), KO ( ), KO+AAV-CAG-EGFP ( ), KO+AAV-CAG-FABP5 SEC ( ), and KO+AAV-CAG-FABP7 ( ). Right panel, Superimposed IPSC traces collected before and during DSI. D 2 , Averaged magnitude of DSI obtained in WT ( : 45.99 ± 2.51%; n = 10 cells; N = 5 mice), KO ( : 5.85 ± 1.21%; n = 17 cells; N = 5 mice), KO+AAV-CAG-EGFP ( : 10.24 ± 1.70%; n = 16 cells; N = 5 mice), KO+AAV-CAG-FABP5 SEC ( : 38.61 ± 1.94%; n = 17 cells; N = 5 mice; p = 9.83x10 −16 versus KO+AAV-CAG-EGFP, p = 0.16 vs. WT), and KO+AAV-CAG-FABP7 ( : 8.10 ± 2.19%; n = 18 cells; N = 5 mice; p = 3.62x10 −19 versus WT, p = 1 versus KO+AAV-CAG-EGFP, p = 8.22x10 −18 versus KO+AAV-CAG-FABP5 SEC ). Scale bars: 100 ms, 200 pA (E and F) Expression of FABP7 in the CA1 region of FABP5 KO mice. e 1 -e 3 , Immunolabelling for FABP7, s100β and merge. Scale bar: 10 μm. f 1 -f 3 , immunolabelling for FABP7, NeuN and merge. Scale bar: 10 μm. Data are represented as mean ± SEM. ∗∗∗ p < 0.001, one-way ANOVA with Bonferroni’s multiple comparisons test.

Journal: iScience

Article Title: Astrocytic FABP5 mediates retrograde endocannabinoid transport at central synapses

doi: 10.1016/j.isci.2025.112342

Figure Lengend Snippet: Extracellular pool of FABP5 mediates hippocampal DSI (A) Secreted FABP5 variant (FABP5 SEC ) binds to 2-AG with comparable affinity to WT FABP5 (FABP5 Ki: 1.0 ± 0.1 μM; FABP5 SEC Ki: 1.6 ± 0.2 μM, n = 4). (B) AAV-mediated expression of FABP5 SEC in CA1 astrocytes of FABP5 KO mice. b 1 -b 3 , Immunolabelling for FABP5, s100β, and merge with DAPI. Scale bar: 10 μm. (C) Neuronal expression of FABP5 SEC in the CA1 region. c 1 -c 3 , Immunolabelling for FABP5, NeuN, and merge with DAPI. Scale bar: 10 μm. (D) Expression of FABP5 SEC but not FABP7 restores DSI in FABP5 KO mice. D 1 , left panel, Summary of the time course of hippocampal DSI recorded from WT ( ), KO ( ), KO+AAV-CAG-EGFP ( ), KO+AAV-CAG-FABP5 SEC ( ), and KO+AAV-CAG-FABP7 ( ). Right panel, Superimposed IPSC traces collected before and during DSI. D 2 , Averaged magnitude of DSI obtained in WT ( : 45.99 ± 2.51%; n = 10 cells; N = 5 mice), KO ( : 5.85 ± 1.21%; n = 17 cells; N = 5 mice), KO+AAV-CAG-EGFP ( : 10.24 ± 1.70%; n = 16 cells; N = 5 mice), KO+AAV-CAG-FABP5 SEC ( : 38.61 ± 1.94%; n = 17 cells; N = 5 mice; p = 9.83x10 −16 versus KO+AAV-CAG-EGFP, p = 0.16 vs. WT), and KO+AAV-CAG-FABP7 ( : 8.10 ± 2.19%; n = 18 cells; N = 5 mice; p = 3.62x10 −19 versus WT, p = 1 versus KO+AAV-CAG-EGFP, p = 8.22x10 −18 versus KO+AAV-CAG-FABP5 SEC ). Scale bars: 100 ms, 200 pA (E and F) Expression of FABP7 in the CA1 region of FABP5 KO mice. e 1 -e 3 , Immunolabelling for FABP7, s100β and merge. Scale bar: 10 μm. f 1 -f 3 , immunolabelling for FABP7, NeuN and merge. Scale bar: 10 μm. Data are represented as mean ± SEM. ∗∗∗ p < 0.001, one-way ANOVA with Bonferroni’s multiple comparisons test.

Techniques: Variant Assay, Expressing

Conditional deletion of hippocampal FABP5 blunts DSI (A) Schematic of the gene structure of FABP5 FLOX mice. (B) Expression of FABP5 and a lack of tdTomato in the hippocampus of FABP5 FLOX mice. Left panel, Immunostaining for DAPI and tdTomato in CA1 region of FABP5 FLOX mice. Right panel, Immunostaining for DAPI and FABP5 in CA1 region of FABP5 FLOX mice. Scale bar: 50 μm. (C) Cre-mediated deletion of FABP5 and expression of tdTomato in the CA1 region of FABP5 FLOX mice. c1-c3, Immunostaining for tdTomato, s100β, and merge. c4-c6, Immunolabeling of tdTomato, NeuN and merge. c7-c9, immunolabeling of tdTomato, FABP5 and merge. Scale bar: 50 μm. (D) Conditional deletion of FABP5 inhibits DSI. Left panel, Averaged magnitude of hippocampal DSI recorded in FABP5 FLOX ( : 41.29 ± 3.54%; n = 11 cells; N = 5 mice), FABP5 FLOX +AAV-CMV-Cre ( : 3.51 ± 1.22%; n = 11 cells; N = 3 mice; p = 3.95×10 −12 versus FABP5 FLOX ), FABP5 FLOX +AAV-CMV-EGFP ( : 34.61 ± 2.93%; n = 11 cells; N = 4 mice; p = 1.44×10 − 9 versus FABP5 FLOX +AAV-CMV-Cre, p = 0.87 versus FABP5 FLOX ). Right panel, representative traces of IPSCs collected before and during DSI from FABP5 FLOX ( ), FABP5 FLOX +AAV-CMV-Cre ( ), and FABP5 FLOX +AAV-CMV-EGFP ( ). Scale bars: 100 ms, 200 pA (E) Averaged time course of the DSI recorded in FABP5 FLOX and FABP5 FLOX +AAV-CMV-EGFP mice. (F) Conditional deletion of FABP5 in the CA1 region does not affect the function of presynaptic CBRs. Left panel, Summary of the depression of IPSC amplitude induced by WIN55,212-2 (10 μM) in FABP5 FLOX ( : 46.13 ± 9.15%; n = 7 cells; N = 4 mice; p = 7.03×10 −5 versus baseline) and FABP5 FLOX +AAV-CMV-Cre ( : 38.76 ± 9.63%; n = 6 cells; N = 4 mice; p = 2.55×10 −5 versus baseline). Right panel, superimposed IPSCs traces collected before and during WIN55,212-2 application. Scale bars: 100 ms, 200 pA. Data are represented as mean ± SEM. ∗∗∗ p < 0.001, one-way ANOVA with Bonferroni’s multiple comparisons test.

Journal: iScience

Article Title: Astrocytic FABP5 mediates retrograde endocannabinoid transport at central synapses

doi: 10.1016/j.isci.2025.112342

Figure Lengend Snippet: Conditional deletion of hippocampal FABP5 blunts DSI (A) Schematic of the gene structure of FABP5 FLOX mice. (B) Expression of FABP5 and a lack of tdTomato in the hippocampus of FABP5 FLOX mice. Left panel, Immunostaining for DAPI and tdTomato in CA1 region of FABP5 FLOX mice. Right panel, Immunostaining for DAPI and FABP5 in CA1 region of FABP5 FLOX mice. Scale bar: 50 μm. (C) Cre-mediated deletion of FABP5 and expression of tdTomato in the CA1 region of FABP5 FLOX mice. c1-c3, Immunostaining for tdTomato, s100β, and merge. c4-c6, Immunolabeling of tdTomato, NeuN and merge. c7-c9, immunolabeling of tdTomato, FABP5 and merge. Scale bar: 50 μm. (D) Conditional deletion of FABP5 inhibits DSI. Left panel, Averaged magnitude of hippocampal DSI recorded in FABP5 FLOX ( : 41.29 ± 3.54%; n = 11 cells; N = 5 mice), FABP5 FLOX +AAV-CMV-Cre ( : 3.51 ± 1.22%; n = 11 cells; N = 3 mice; p = 3.95×10 −12 versus FABP5 FLOX ), FABP5 FLOX +AAV-CMV-EGFP ( : 34.61 ± 2.93%; n = 11 cells; N = 4 mice; p = 1.44×10 − 9 versus FABP5 FLOX +AAV-CMV-Cre, p = 0.87 versus FABP5 FLOX ). Right panel, representative traces of IPSCs collected before and during DSI from FABP5 FLOX ( ), FABP5 FLOX +AAV-CMV-Cre ( ), and FABP5 FLOX +AAV-CMV-EGFP ( ). Scale bars: 100 ms, 200 pA (E) Averaged time course of the DSI recorded in FABP5 FLOX and FABP5 FLOX +AAV-CMV-EGFP mice. (F) Conditional deletion of FABP5 in the CA1 region does not affect the function of presynaptic CBRs. Left panel, Summary of the depression of IPSC amplitude induced by WIN55,212-2 (10 μM) in FABP5 FLOX ( : 46.13 ± 9.15%; n = 7 cells; N = 4 mice; p = 7.03×10 −5 versus baseline) and FABP5 FLOX +AAV-CMV-Cre ( : 38.76 ± 9.63%; n = 6 cells; N = 4 mice; p = 2.55×10 −5 versus baseline). Right panel, superimposed IPSCs traces collected before and during WIN55,212-2 application. Scale bars: 100 ms, 200 pA. Data are represented as mean ± SEM. ∗∗∗ p < 0.001, one-way ANOVA with Bonferroni’s multiple comparisons test.

Techniques: Expressing, Immunostaining, Immunolabeling

Deletion of astrocytic FABP5 impairs hippocampal DSI (A) Schematic showing the experimental strategy used to delete astrocytic FABP5 and generate FABP5 FLOX /Aldh1l1 Cre mice. FABP5 FLOX /Aldh1l1 Cre /Tam represent tamoxifen-injected FABP5 FLOX /Aldh1l1 Cre mice, FABP5 FLOX /Aldh1l1/Tam represent tamoxifen-injected Cre − littermates, while FABP5 FLOX /Aldh1l1 Cre mice received vehicle. (B) Tamoxifen-induced deletion of the FABP5 and expression of tdTomato in astrocytes in the CA1 region of FABP5 FLOX /Aldh1l1 Cre /Tam mice. b1-b3, Images of tdTomato, NeuN staining, and merge. b4-b6, Images of tdTomato, s100β, and merge. b7-b9, images of immunostaining for tdTomato, FABP5, and merge. Note the expression of tdTomato in astrocytes but not in neurons and the absence of FABP5 expression. Scale bars: 50 μm. (C) Tamoxifen-induced deletion of FABP5 impairs DSI in FABP5 FLOX /Aldh1l1 Cre /Tam mice. Left panel, Averaged DSI magnitude obtained in FABP5 FLOX /Aldh1l1 Cre ( : 38.12 ± 2.97%; n = 16 cells; N = 4 mice), in FABP5 FLOX/ Aldh1l1/Tam ( : 32.12 ± 2.50%; n = 15 cells; N = 4 mice; p = 0.27 versus FABP5 FLOX /Aldh1l1 Cre ) and in FABP5 FLOX /Aldh1l1 Cre /Tam ( : 6.32 ± 1.85%; n = 14 cells; N = 4 mice; p = 2.22×10 −8 versus FABP5 FLOX /Aldh1l1/Tam). Right panel, Superimposed IPSC traces collected before and during DSI from FABP5 FLOX /Aldh1l1 Cre ( ), FABP5 FLOX /Aldh1l1/Tam ( ), and FABP5 FLOX /Aldh1l1 Cre /Tam ( ) mice. Scale bars: 100 ms, 200 pA. (D) Averaged time course of DSI recorded from FABP5 FLOX /Aldh1l1 Cre ( ), FABP5 FLOX /Aldh1l1/Tam ( ), and FABP5 FLOX /Aldh1l1 Cre /Tam ( ) mice. (E) Deletion of astrocytic FABP5 does not affect the function of CB1Rs. Summary of the depression of IPSC amplitude induced by WIN55,212-2 (10 μM) in FABP5 FLOX /Aldh1l1 Cre ( :44.75 ± 3.73%; n = 5 cells; N = 3 mice; p = 2.52×10 − 6 versus baseline) and FABP5 FLOX /Aldh1l1 Cre /Tam ( : 54.74 ± 8.11%; n = 5 cells; N = 3 mice; p = 2.29×10 − 5 versus baseline). Right panel, Sample IPSCs traces collected before and during WIN55,212-2 application. Scale bars: 100 ms, 100 pA. Data are represented as mean ± SEM. ∗∗∗ p < 0.001, one-way ANOVA with Bonferroni’s multiple comparisons test.

Journal: iScience

Article Title: Astrocytic FABP5 mediates retrograde endocannabinoid transport at central synapses

doi: 10.1016/j.isci.2025.112342

Figure Lengend Snippet: Deletion of astrocytic FABP5 impairs hippocampal DSI (A) Schematic showing the experimental strategy used to delete astrocytic FABP5 and generate FABP5 FLOX /Aldh1l1 Cre mice. FABP5 FLOX /Aldh1l1 Cre /Tam represent tamoxifen-injected FABP5 FLOX /Aldh1l1 Cre mice, FABP5 FLOX /Aldh1l1/Tam represent tamoxifen-injected Cre − littermates, while FABP5 FLOX /Aldh1l1 Cre mice received vehicle. (B) Tamoxifen-induced deletion of the FABP5 and expression of tdTomato in astrocytes in the CA1 region of FABP5 FLOX /Aldh1l1 Cre /Tam mice. b1-b3, Images of tdTomato, NeuN staining, and merge. b4-b6, Images of tdTomato, s100β, and merge. b7-b9, images of immunostaining for tdTomato, FABP5, and merge. Note the expression of tdTomato in astrocytes but not in neurons and the absence of FABP5 expression. Scale bars: 50 μm. (C) Tamoxifen-induced deletion of FABP5 impairs DSI in FABP5 FLOX /Aldh1l1 Cre /Tam mice. Left panel, Averaged DSI magnitude obtained in FABP5 FLOX /Aldh1l1 Cre ( : 38.12 ± 2.97%; n = 16 cells; N = 4 mice), in FABP5 FLOX/ Aldh1l1/Tam ( : 32.12 ± 2.50%; n = 15 cells; N = 4 mice; p = 0.27 versus FABP5 FLOX /Aldh1l1 Cre ) and in FABP5 FLOX /Aldh1l1 Cre /Tam ( : 6.32 ± 1.85%; n = 14 cells; N = 4 mice; p = 2.22×10 −8 versus FABP5 FLOX /Aldh1l1/Tam). Right panel, Superimposed IPSC traces collected before and during DSI from FABP5 FLOX /Aldh1l1 Cre ( ), FABP5 FLOX /Aldh1l1/Tam ( ), and FABP5 FLOX /Aldh1l1 Cre /Tam ( ) mice. Scale bars: 100 ms, 200 pA. (D) Averaged time course of DSI recorded from FABP5 FLOX /Aldh1l1 Cre ( ), FABP5 FLOX /Aldh1l1/Tam ( ), and FABP5 FLOX /Aldh1l1 Cre /Tam ( ) mice. (E) Deletion of astrocytic FABP5 does not affect the function of CB1Rs. Summary of the depression of IPSC amplitude induced by WIN55,212-2 (10 μM) in FABP5 FLOX /Aldh1l1 Cre ( :44.75 ± 3.73%; n = 5 cells; N = 3 mice; p = 2.52×10 − 6 versus baseline) and FABP5 FLOX /Aldh1l1 Cre /Tam ( : 54.74 ± 8.11%; n = 5 cells; N = 3 mice; p = 2.29×10 − 5 versus baseline). Right panel, Sample IPSCs traces collected before and during WIN55,212-2 application. Scale bars: 100 ms, 100 pA. Data are represented as mean ± SEM. ∗∗∗ p < 0.001, one-way ANOVA with Bonferroni’s multiple comparisons test.

Techniques: Injection, Expressing, Staining, Immunostaining

Expression of FABP5 in astrocytes of FABP5 KO mice rescues DSI (A) AAV-mediated expression of FABP5 under the control of the gfaABC1D promoter in FABP5 KO mice. a1-a3, Immunostaining of FABP5, s100β and merge. Scale bar: 50 μm. a4, Co-localization of FABP5 with s100β. a5, Lack of co-localization of FABP5 with NeuN. Scale bars: 10 μm. (B) Expression of FABP5 in astrocytes rescues DSI in FABP5 KO mice. Left panel, averaged magnitude of DSI obtained in WT ( : 42.23 ± 3.44%; n = 12 cells; N = 3 mice), KO ( : 2.65 ± 1.03%; n = 13 cells; N = 3 mice; p = 3.28×10 −13 versus WT), KO+AAV-gfaABC1D-FABP5 ( : 33.37 ± 3.50%; n = 13 cells; N = 4 mice; p = 0.12 versus WT), and KO+AAV-GFAP-EGFP ( : 6.07 ± 1.58%; n = 12 cells; N = 4 mice; p = 1.71×10 − 8 versus KO+AAV-gfaABC1D-FABP5). Right panel, IPSC traces collected before and during DSI from WT ( ), KO ( ), KO+AAV-gfaABC1D-FABP5 ( ), and KO+AAV-GFAP-EGFP ( ). Scale bars: 100 ms, 200 pA. (C) AAV-mediated expression of FABP5 under the neuron-specific hsynapsin1 promoter in FABP5 KO mice. c1-c3, Immunostaining for NeuN, FABP5, and merge. Scale bar: 50 μm. c4, Co-localization of FABP5 with NeuN. c5, Lack of co-localization of FABP5 with s100β. Scale bars: 10 μm. (D) Expression of FABP5 in neurons partially rescues DSI in FABP5 KO mice. Left panel, Summary of DSI magnitude recorded from WT ( : 39.52 ± 1.65%; n = 11 cells; N = 5 mice), KO ( : 1.43 ± 0.66%; n = 11 cells; N = 4 mice; p = 4.67×10 −18 versus WT), KO+AAV-hSyn-FABP5 ( : 13.95 ± 2.13%; n = 15 cells; N = 5 mice; p = 4.47×10 −13 versus WT) and KO+AAV-hSyn-EGFP ( : 5.15 ± 1.61%; n = 12 cells; N = 4 mice; p = 0.89 versus KO). Right panel, IPSC traces collected before and during DSI. Data are represented as mean ± SEM. ∗ p < 0.05; ∗∗∗ p < 0.001, one-way ANOVA with Bonferroni’s multiple comparisons test.

Journal: iScience

Article Title: Astrocytic FABP5 mediates retrograde endocannabinoid transport at central synapses

doi: 10.1016/j.isci.2025.112342

Figure Lengend Snippet: Expression of FABP5 in astrocytes of FABP5 KO mice rescues DSI (A) AAV-mediated expression of FABP5 under the control of the gfaABC1D promoter in FABP5 KO mice. a1-a3, Immunostaining of FABP5, s100β and merge. Scale bar: 50 μm. a4, Co-localization of FABP5 with s100β. a5, Lack of co-localization of FABP5 with NeuN. Scale bars: 10 μm. (B) Expression of FABP5 in astrocytes rescues DSI in FABP5 KO mice. Left panel, averaged magnitude of DSI obtained in WT ( : 42.23 ± 3.44%; n = 12 cells; N = 3 mice), KO ( : 2.65 ± 1.03%; n = 13 cells; N = 3 mice; p = 3.28×10 −13 versus WT), KO+AAV-gfaABC1D-FABP5 ( : 33.37 ± 3.50%; n = 13 cells; N = 4 mice; p = 0.12 versus WT), and KO+AAV-GFAP-EGFP ( : 6.07 ± 1.58%; n = 12 cells; N = 4 mice; p = 1.71×10 − 8 versus KO+AAV-gfaABC1D-FABP5). Right panel, IPSC traces collected before and during DSI from WT ( ), KO ( ), KO+AAV-gfaABC1D-FABP5 ( ), and KO+AAV-GFAP-EGFP ( ). Scale bars: 100 ms, 200 pA. (C) AAV-mediated expression of FABP5 under the neuron-specific hsynapsin1 promoter in FABP5 KO mice. c1-c3, Immunostaining for NeuN, FABP5, and merge. Scale bar: 50 μm. c4, Co-localization of FABP5 with NeuN. c5, Lack of co-localization of FABP5 with s100β. Scale bars: 10 μm. (D) Expression of FABP5 in neurons partially rescues DSI in FABP5 KO mice. Left panel, Summary of DSI magnitude recorded from WT ( : 39.52 ± 1.65%; n = 11 cells; N = 5 mice), KO ( : 1.43 ± 0.66%; n = 11 cells; N = 4 mice; p = 4.67×10 −18 versus WT), KO+AAV-hSyn-FABP5 ( : 13.95 ± 2.13%; n = 15 cells; N = 5 mice; p = 4.47×10 −13 versus WT) and KO+AAV-hSyn-EGFP ( : 5.15 ± 1.61%; n = 12 cells; N = 4 mice; p = 0.89 versus KO). Right panel, IPSC traces collected before and during DSI. Data are represented as mean ± SEM. ∗ p < 0.05; ∗∗∗ p < 0.001, one-way ANOVA with Bonferroni’s multiple comparisons test.

Techniques: Expressing, Control, Immunostaining

Journal: iScience

Article Title: Astrocytic FABP5 mediates retrograde endocannabinoid transport at central synapses

doi: 10.1016/j.isci.2025.112342

Figure Lengend Snippet:

Techniques: Virus, Recombinant, Software, Imaging, Transfection, Real-time Polymerase Chain Reaction, SYBR Green Assay, Mass Spectrometry, Control, Microscopy

Proteins detected by western blot and antibodies used.

Journal: International Journal of Oncology

Article Title: FABP5 can substitute for androgen receptor in malignant progression of prostate cancer cells

doi: 10.3892/ijo.2023.5606

Figure Lengend Snippet: Proteins detected by western blot and antibodies used.

Article Snippet: FABP5 , Monoclonal Rabbit Anti-human FABP5 (1:500; Hycult; cat. no. HP-9030) , Swine polyclonal anti-rabbit Immunoglobulin/HRP (Dako; Agilent Technologies, Inc.; 1:20,000; cat no: P039901-2).

Techniques: Western Blot, Marker

The guide RNAs, PAM sequences, and the genomic locations of the KO genes.

Journal: International Journal of Oncology

Article Title: FABP5 can substitute for androgen receptor in malignant progression of prostate cancer cells

doi: 10.3892/ijo.2023.5606

Figure Lengend Snippet: The guide RNAs, PAM sequences, and the genomic locations of the KO genes.

Techniques:

Western blot analysis of some key proteins associated with the FABP5 pathway in benign and malignant prostate cells, and western blot analysis was combined with DNA-sequencing analysis to verify the successful gene KO cell clones. An anti-β-actin antibody was incubated with each blot to standardize the immunological responses. Quantitative analysis was performed by densitometrical scanning of the area and peak of each band on the blot. The protein relative levels were reproduced independently three times, and the differences were assessed by Student's t-test for results with 2 datasets, and one-way ANOVA test for results with 3 or more datasets. Dunnett's post hoc test was utilized for multiple comparisons following the ANOVA. (A) Relative expression of FABP5 pathway-associated proteins in benign and malignant prostate epithelial cells is shown. a) Western blot analysis of FABP5 in benign PNT2 cells, the moderately malignant 22RV1 cells, and the highly malignant prostate carcinoma cell lines, DU145 and PC3M. b) Relative levels of FABP5 protein in PNT2, 22RV1, DU145 and PC3M cells. The level of FABP5 in 22RV1 cells was set at '1', and the levels in DU145 and PC3M were obtained by comparing with that of 22RV1. c) Western blot detection of PPARγ in PNT2, 22RV1, DU145 and PC3M cells. d) Relative levels of PPARγ in PNT2, 22RV1, DU145, and PC3M cells. The level in PNT2 cells was set at '1', and the levels in the other cell lines were obtained by comparing with that of PNT2. e) Western blot analysis of pPPARγ in PNT2, 22RV1, DU145 and PC3M cells. f) Relative levels of pPPARγ in PNT2, 22RV1, DU145, and PC3M cells. The level in 22RV1 cells was set at '1', and levels in DU145 and PC3M were obtained by comparing with that of 22RV1. g) Western blot analysis of ARFL protein in PNT2, 22RV1, DU145 and PC3M cells. h) Relative levels of ARFL in prostate cell lines. The level of ARFL in 22RV1 cells was set at '1', and levels in the other cell lines were not detectable. i) Western blot analysis of VEGF protein in PNT2, 22RV1, DU145 and PC3M cells. j) Relative levels of VEGF; the level in PNT2 was set at '1', and levels in the other cell lines were obtained by comparing with that of PNT2. (B) Western blot and DNA sequencing analyses were performed to verify successful gene suppression in KO cell clones. a) Western blots of FABP5 protein in 22RV1 cells and its derivative FABP5 -KO clones. b) Relative levels of FABP5 in 22RV1 cells and in its derivative FABP5 -KO clones. The level of FABP5 in 22RV1 cells was set at '1', and levels in different clones were obtained by comparing with that in 22RV1. c) Further Western blots of FABP5 protein in 22RV1 cells and in the successful FABP5 -KO clone C3. d) DNA sequence analysis revealed the location where the guide RNA-induced mutation occurred (depicted by the black arrow). e) Western blot analysis of FABP5 protein in DU145 cells and in its derivative FABP5 -KO clones. f) Relative levels of FABP5 in DU145 and in the different FABP5 -KO clones. The level of FABP5 in DU145 was set at '1', and the levels in the different clones were obtained by comparing with that in DU145. g) Western blot analysis of FABP5 protein in DU145 cells and in a selected FABP5 -KO clone (C2). h) DNA sequence analysis revealed the location where the guide RNA-induced mutation occurred (depicted by the black arrow). i) Western blot detection of FABP5 expression in PC3M and in different FABP5 -KO clones. j) Relative levels of FABP5 in PC3M and in its different FABP5 -KO clones. The level of FABP5 in PC3M was set at '1', and the levels in its different FABP5 -KO clones were obtained by comparing with that in PC3M. k) Western blot analysis of FABP5 protein in PC3M and in its selected FABP5 -KO clone, C6. l) DNA sequence analysis revealed the location where the guide RNA-induced mutation occurred (depicted by the black arrow). m) Western blot analysis of AR protein in 22RV1 cells and in its different AR -KO clones. n) Relative levels of AR in 22RV1 cells and in its AR -KO clones. The level of AR in 22RV1 was set at '1', and the levels of AR in different clones were obtained by comparing with that in 22RV1. o) Western blot analysis of AR expression in 22RV1 cells and in its AR -KO clones. p) Relative levels of AR in 22RV1 and in its AR -KO clones. The level of AR in 22RV1 was set at '1', and the levels of AR in different clones were obtained by comparing with that in 22RV1 cells. *** P<0.0001 and **** P<0.00001. KO, knockout; FABP5, fatty acid-binding protein 5; AR, androgen receptor; PPARγ, peroxisome proliferator-activated receptor-γ; VEGF, vascular endothelium growth factor; pPPARγ, phosphorylated PPARγ; ns, not statistically significant.

Journal: International Journal of Oncology

Article Title: FABP5 can substitute for androgen receptor in malignant progression of prostate cancer cells

doi: 10.3892/ijo.2023.5606

Figure Lengend Snippet: Western blot analysis of some key proteins associated with the FABP5 pathway in benign and malignant prostate cells, and western blot analysis was combined with DNA-sequencing analysis to verify the successful gene KO cell clones. An anti-β-actin antibody was incubated with each blot to standardize the immunological responses. Quantitative analysis was performed by densitometrical scanning of the area and peak of each band on the blot. The protein relative levels were reproduced independently three times, and the differences were assessed by Student's t-test for results with 2 datasets, and one-way ANOVA test for results with 3 or more datasets. Dunnett's post hoc test was utilized for multiple comparisons following the ANOVA. (A) Relative expression of FABP5 pathway-associated proteins in benign and malignant prostate epithelial cells is shown. a) Western blot analysis of FABP5 in benign PNT2 cells, the moderately malignant 22RV1 cells, and the highly malignant prostate carcinoma cell lines, DU145 and PC3M. b) Relative levels of FABP5 protein in PNT2, 22RV1, DU145 and PC3M cells. The level of FABP5 in 22RV1 cells was set at '1', and the levels in DU145 and PC3M were obtained by comparing with that of 22RV1. c) Western blot detection of PPARγ in PNT2, 22RV1, DU145 and PC3M cells. d) Relative levels of PPARγ in PNT2, 22RV1, DU145, and PC3M cells. The level in PNT2 cells was set at '1', and the levels in the other cell lines were obtained by comparing with that of PNT2. e) Western blot analysis of pPPARγ in PNT2, 22RV1, DU145 and PC3M cells. f) Relative levels of pPPARγ in PNT2, 22RV1, DU145, and PC3M cells. The level in 22RV1 cells was set at '1', and levels in DU145 and PC3M were obtained by comparing with that of 22RV1. g) Western blot analysis of ARFL protein in PNT2, 22RV1, DU145 and PC3M cells. h) Relative levels of ARFL in prostate cell lines. The level of ARFL in 22RV1 cells was set at '1', and levels in the other cell lines were not detectable. i) Western blot analysis of VEGF protein in PNT2, 22RV1, DU145 and PC3M cells. j) Relative levels of VEGF; the level in PNT2 was set at '1', and levels in the other cell lines were obtained by comparing with that of PNT2. (B) Western blot and DNA sequencing analyses were performed to verify successful gene suppression in KO cell clones. a) Western blots of FABP5 protein in 22RV1 cells and its derivative FABP5 -KO clones. b) Relative levels of FABP5 in 22RV1 cells and in its derivative FABP5 -KO clones. The level of FABP5 in 22RV1 cells was set at '1', and levels in different clones were obtained by comparing with that in 22RV1. c) Further Western blots of FABP5 protein in 22RV1 cells and in the successful FABP5 -KO clone C3. d) DNA sequence analysis revealed the location where the guide RNA-induced mutation occurred (depicted by the black arrow). e) Western blot analysis of FABP5 protein in DU145 cells and in its derivative FABP5 -KO clones. f) Relative levels of FABP5 in DU145 and in the different FABP5 -KO clones. The level of FABP5 in DU145 was set at '1', and the levels in the different clones were obtained by comparing with that in DU145. g) Western blot analysis of FABP5 protein in DU145 cells and in a selected FABP5 -KO clone (C2). h) DNA sequence analysis revealed the location where the guide RNA-induced mutation occurred (depicted by the black arrow). i) Western blot detection of FABP5 expression in PC3M and in different FABP5 -KO clones. j) Relative levels of FABP5 in PC3M and in its different FABP5 -KO clones. The level of FABP5 in PC3M was set at '1', and the levels in its different FABP5 -KO clones were obtained by comparing with that in PC3M. k) Western blot analysis of FABP5 protein in PC3M and in its selected FABP5 -KO clone, C6. l) DNA sequence analysis revealed the location where the guide RNA-induced mutation occurred (depicted by the black arrow). m) Western blot analysis of AR protein in 22RV1 cells and in its different AR -KO clones. n) Relative levels of AR in 22RV1 cells and in its AR -KO clones. The level of AR in 22RV1 was set at '1', and the levels of AR in different clones were obtained by comparing with that in 22RV1. o) Western blot analysis of AR expression in 22RV1 cells and in its AR -KO clones. p) Relative levels of AR in 22RV1 and in its AR -KO clones. The level of AR in 22RV1 was set at '1', and the levels of AR in different clones were obtained by comparing with that in 22RV1 cells. *** P<0.0001 and **** P<0.00001. KO, knockout; FABP5, fatty acid-binding protein 5; AR, androgen receptor; PPARγ, peroxisome proliferator-activated receptor-γ; VEGF, vascular endothelium growth factor; pPPARγ, phosphorylated PPARγ; ns, not statistically significant.

Techniques: Western Blot, DNA Sequencing, Clone Assay, Incubation, Expressing, Sequencing, Mutagenesis, Knock-Out, Binding Assay

Effect of FABP5 -KO on malignant characteristics of 22RV1 cells and on the levels of downstream proteins of the FABP5 signaling pathway. (A) Microscopical appearances of 22RV1-FABP5-KO cells and their parental 22RV1 cells. (B) Effect of FABP5 -KO on proliferation of 22RV1 cells. C) Effect of FABP5 -KO on invasion of 22RV1 cells. (D) Quantitative assessment of the numbers of invasive cells. (E) Effect of FABP5 -KO on anchorage-independent growth of 22RV1 cells. (F) Quantitative assessment on cell colony numbers formed in soft agar. (G) Effect of FABP5 -KO on motility of 22RV1 cells. (H) Quantitative assessment of the average wound width of the space of the gap ( μ m) at different times is shown. (I) Western blot analysis of PPARγ1 and PPARγ2 in 22RV1 and in 22RV1-FABP5-KO cells. (J) Relative levels of PPARγ1 and PPARγ2. The levels of PPARγ1 and PPARγ2 in 22RV1 cells were each set at '1', and their levels in 22RV1-FABP5-KO cells were obtained by comparing with those in 22RV1. (K) Western blot analysis of pPPARγ1 and pPPARγ2 in 22RV1 and in 22RV1-FABP5-KO cells. (L) Relative levels of pPPARγ1 and pPPARγ2. The levels of pPPARγ1 and pPPARγ2 in 22RV1 were each set at '1', and those in 22RV1-FABP5-KO cells were obtained by comparing with those in 22RV1. (M) Western blot analysis of VEGF in 22RV1 and in 22RV1-FABP5-KO cells. (N) Relative levels of VEGF protein. The level of VEGF in 22RV1 cells was set at '1', and the level of VEGF in 22RV1-FABP5-KO cells was obtained by comparing with that in 22RV1. (O) Western blot analysis of ARFL and ARV7 in 22RV1 and in 22RV1-FABP5-KO cells. (P) Relative levels of ARFL and ARV7. Levels of ARFL and ARV7 in 22RV1 cells were set at '1', and the levels of ARFL and ARV7 in 22RV1-FABP5-KO cells were obtained by comparing with those in 22RV1. The protein relative levels were reproduced independently three times, and the differences were assessed by Student's t-test. Results were considered significant when P<0.05. ** P<0.001, *** P<0.0001 and **** P<0.00001. KO, knockout; FABP5, fatty acid-binding protein 5; AR, androgen receptor; ARFL, full-length AR; ARV7, AR splicing variant 7; PPARγ, peroxisome proliferator-activated receptor-γ; pPPARγ, phosphorylated PPARγ; ns, not statistically significant.

Journal: International Journal of Oncology

Article Title: FABP5 can substitute for androgen receptor in malignant progression of prostate cancer cells

doi: 10.3892/ijo.2023.5606

Figure Lengend Snippet: Effect of FABP5 -KO on malignant characteristics of 22RV1 cells and on the levels of downstream proteins of the FABP5 signaling pathway. (A) Microscopical appearances of 22RV1-FABP5-KO cells and their parental 22RV1 cells. (B) Effect of FABP5 -KO on proliferation of 22RV1 cells. C) Effect of FABP5 -KO on invasion of 22RV1 cells. (D) Quantitative assessment of the numbers of invasive cells. (E) Effect of FABP5 -KO on anchorage-independent growth of 22RV1 cells. (F) Quantitative assessment on cell colony numbers formed in soft agar. (G) Effect of FABP5 -KO on motility of 22RV1 cells. (H) Quantitative assessment of the average wound width of the space of the gap ( μ m) at different times is shown. (I) Western blot analysis of PPARγ1 and PPARγ2 in 22RV1 and in 22RV1-FABP5-KO cells. (J) Relative levels of PPARγ1 and PPARγ2. The levels of PPARγ1 and PPARγ2 in 22RV1 cells were each set at '1', and their levels in 22RV1-FABP5-KO cells were obtained by comparing with those in 22RV1. (K) Western blot analysis of pPPARγ1 and pPPARγ2 in 22RV1 and in 22RV1-FABP5-KO cells. (L) Relative levels of pPPARγ1 and pPPARγ2. The levels of pPPARγ1 and pPPARγ2 in 22RV1 were each set at '1', and those in 22RV1-FABP5-KO cells were obtained by comparing with those in 22RV1. (M) Western blot analysis of VEGF in 22RV1 and in 22RV1-FABP5-KO cells. (N) Relative levels of VEGF protein. The level of VEGF in 22RV1 cells was set at '1', and the level of VEGF in 22RV1-FABP5-KO cells was obtained by comparing with that in 22RV1. (O) Western blot analysis of ARFL and ARV7 in 22RV1 and in 22RV1-FABP5-KO cells. (P) Relative levels of ARFL and ARV7. Levels of ARFL and ARV7 in 22RV1 cells were set at '1', and the levels of ARFL and ARV7 in 22RV1-FABP5-KO cells were obtained by comparing with those in 22RV1. The protein relative levels were reproduced independently three times, and the differences were assessed by Student's t-test. Results were considered significant when P<0.05. ** P<0.001, *** P<0.0001 and **** P<0.00001. KO, knockout; FABP5, fatty acid-binding protein 5; AR, androgen receptor; ARFL, full-length AR; ARV7, AR splicing variant 7; PPARγ, peroxisome proliferator-activated receptor-γ; pPPARγ, phosphorylated PPARγ; ns, not statistically significant.

Techniques: Western Blot, Knock-Out, Binding Assay, Variant Assay

Effect of AR -KO on the malignant characteristics of 22RV1 cells and on levels of the down-stream proteins of the FABP5 signalling pathway. (A) Microscopical appearances of 22RV1 and 22RV1-AR-KO. (B) Effect of AR -KO on proliferation of 22RV1 and 22RV1-AR-KO cells. (C) Effect of AR -KO on 22RV1 cell invasion. (D) Average number of invasive cells from 22RV1 and 22RV1-AR-KO cells. (E) Effect of AR knockout on anchorage-independent growth of 22RV1 cells. (F) Relative numbers of colonies formed in soft agar by 22RV1 and 22RV1-AR-KO cells. (G) Effect of AR -KO on gap closure of 22RV1 and 22RV1-AR-KO cells. (H) Quantitative assessment of average sizes of the wound space or gap in 22RV1 and 22RV1-AR-KO cells in μ m at different times. (I) Western blot analysis of PPARγ1 and PPARγ2 in 22RV1 and 22RV1-AR-KO cells. (J) Relative levels of PPARγ1 and PPARγ2 in 22RV1 and 22RV1-AR-KO cells. (K) Western blot analysis of pPPARγ1 and pPPARγ2 in 22RV1 and 22RV1-AR-KO cells. (L) Quantitative assessment of levels of pPPARγ1 and pPPARγ2 proteins. Levels of pPPARγ1 and pPPARγ2 in 22RV1 were set at '1', and the levels in 22RV1AR-KO cells were obtained by comparing with those in 22RV1. (M) Western blot analysis of VEGF in 22RV1 and 22RV1-AR-KO cells. (N) Relative levels of VEGF in 22RV1 and 22RV1-AR-KO cells. The level of VEGF in 22RV1 cells was set at '1', and that in 22RV1-AR-KO cells was obtained by comparing with that in 22RV1. (O) Western blot detection of FABP5 protein in 22RV1 and 22RV1-AR-KO cells (no quantification was made, since the level in 22RV1-FABP5-KO cells was negligible). The protein relative levels were reproduced independently three times, and the differences were assessed by Student's t-test. * P<0.05, *** P<0.0001 and **** P<0.00001. KO, knockout; FABP5, fatty acid-binding protein 5; AR, androgen receptor; PPARγ, peroxisome proliferator-activated receptor-γ; pPPARγ, phosphorylated PPARγ; VEGF, vascular endothelium growth factor; ns, not statistically significant.

Journal: International Journal of Oncology

Article Title: FABP5 can substitute for androgen receptor in malignant progression of prostate cancer cells

doi: 10.3892/ijo.2023.5606

Figure Lengend Snippet: Effect of AR -KO on the malignant characteristics of 22RV1 cells and on levels of the down-stream proteins of the FABP5 signalling pathway. (A) Microscopical appearances of 22RV1 and 22RV1-AR-KO. (B) Effect of AR -KO on proliferation of 22RV1 and 22RV1-AR-KO cells. (C) Effect of AR -KO on 22RV1 cell invasion. (D) Average number of invasive cells from 22RV1 and 22RV1-AR-KO cells. (E) Effect of AR knockout on anchorage-independent growth of 22RV1 cells. (F) Relative numbers of colonies formed in soft agar by 22RV1 and 22RV1-AR-KO cells. (G) Effect of AR -KO on gap closure of 22RV1 and 22RV1-AR-KO cells. (H) Quantitative assessment of average sizes of the wound space or gap in 22RV1 and 22RV1-AR-KO cells in μ m at different times. (I) Western blot analysis of PPARγ1 and PPARγ2 in 22RV1 and 22RV1-AR-KO cells. (J) Relative levels of PPARγ1 and PPARγ2 in 22RV1 and 22RV1-AR-KO cells. (K) Western blot analysis of pPPARγ1 and pPPARγ2 in 22RV1 and 22RV1-AR-KO cells. (L) Quantitative assessment of levels of pPPARγ1 and pPPARγ2 proteins. Levels of pPPARγ1 and pPPARγ2 in 22RV1 were set at '1', and the levels in 22RV1AR-KO cells were obtained by comparing with those in 22RV1. (M) Western blot analysis of VEGF in 22RV1 and 22RV1-AR-KO cells. (N) Relative levels of VEGF in 22RV1 and 22RV1-AR-KO cells. The level of VEGF in 22RV1 cells was set at '1', and that in 22RV1-AR-KO cells was obtained by comparing with that in 22RV1. (O) Western blot detection of FABP5 protein in 22RV1 and 22RV1-AR-KO cells (no quantification was made, since the level in 22RV1-FABP5-KO cells was negligible). The protein relative levels were reproduced independently three times, and the differences were assessed by Student's t-test. * P<0.05, *** P<0.0001 and **** P<0.00001. KO, knockout; FABP5, fatty acid-binding protein 5; AR, androgen receptor; PPARγ, peroxisome proliferator-activated receptor-γ; pPPARγ, phosphorylated PPARγ; VEGF, vascular endothelium growth factor; ns, not statistically significant.

Techniques: Knock-Out, Western Blot, Binding Assay

Effect of FABP5 -KO on the malignant characteristics of DU145 and on protein levels of the downstream proteins of the FABP5 pathway. (A) Microscopical appearances revealed morphological difference between DU145 and DU145-FABP5-KO cells. (B) Effect of FABP5 -KO on the proliferation of DU145 cells. (C) Effect of FABP5 -KO on DU145 cell invasion was assessed by an invasion assay, and (D) the average number of invasive cells from DU145 and DU145-FABP5-KO cells were recorded. (E) Anchorage-independent growth of DU145 and DU145-FABP5-KO cells, and (F) their average colony numbers formed in soft agar. (G) Effect of FABP5 -KO on migration was assessed at different times in a gap closure assay. (H) The quantitative assessment of the average size of wound space gap at different times. (I) Western blot analysis of PPARγ1 and PPARγ2 proteins. (J) Relative levels of PPARγ1 and PPARγ2 in DU145 and DU145-FABP5-KO cells. (K) Western blots were performed for pPPARγ1 and pPPARγ2 in DU145 and DU145-FABP5-KO cells. (L) Relative levels of pPPARγ1 and pPPARγ2. Levels of pPPARγ1 and pPPARγ2 in DU145 cells were each set at '1', and the levels in DU145-FABP5-KO cells were obtained by comparing with those in DU145. (M) Western blot analysis of VEGF protein in DU145 and DU145-FABP5-KO cells. (N) Relative levels of VEGF in DU145 and DU145-FABP5-KO cells; the level of VEGF in DU145 cells was set at '1', and the level in DU145-FABP5-KO cells was obtained by comparing with that in DU145. (O) Western blot analysis of ARFL and ARV7 proteins in DU145 and DU145-FABP5-KO cells. Since neither of the proteins were detectable in either cell line, no quantification was possible. The relative protein levels were reproduced independently three times, and the differences were assessed by Student's t-test. *** P<0.0001 and **** P<0.00001. KO, knockout; FABP5, fatty acid-binding protein 5; AR, androgen receptor; ARFL, full-length AR; ARV7, AR splicing variant 7; PPARγ, peroxisome proliferator-activated receptor-γ; pPPARγ, phosphorylated PPARγ; VEGF, vascular endothelium growth factor; ns, not statistically significant.

Journal: International Journal of Oncology

Article Title: FABP5 can substitute for androgen receptor in malignant progression of prostate cancer cells

doi: 10.3892/ijo.2023.5606

Figure Lengend Snippet: Effect of FABP5 -KO on the malignant characteristics of DU145 and on protein levels of the downstream proteins of the FABP5 pathway. (A) Microscopical appearances revealed morphological difference between DU145 and DU145-FABP5-KO cells. (B) Effect of FABP5 -KO on the proliferation of DU145 cells. (C) Effect of FABP5 -KO on DU145 cell invasion was assessed by an invasion assay, and (D) the average number of invasive cells from DU145 and DU145-FABP5-KO cells were recorded. (E) Anchorage-independent growth of DU145 and DU145-FABP5-KO cells, and (F) their average colony numbers formed in soft agar. (G) Effect of FABP5 -KO on migration was assessed at different times in a gap closure assay. (H) The quantitative assessment of the average size of wound space gap at different times. (I) Western blot analysis of PPARγ1 and PPARγ2 proteins. (J) Relative levels of PPARγ1 and PPARγ2 in DU145 and DU145-FABP5-KO cells. (K) Western blots were performed for pPPARγ1 and pPPARγ2 in DU145 and DU145-FABP5-KO cells. (L) Relative levels of pPPARγ1 and pPPARγ2. Levels of pPPARγ1 and pPPARγ2 in DU145 cells were each set at '1', and the levels in DU145-FABP5-KO cells were obtained by comparing with those in DU145. (M) Western blot analysis of VEGF protein in DU145 and DU145-FABP5-KO cells. (N) Relative levels of VEGF in DU145 and DU145-FABP5-KO cells; the level of VEGF in DU145 cells was set at '1', and the level in DU145-FABP5-KO cells was obtained by comparing with that in DU145. (O) Western blot analysis of ARFL and ARV7 proteins in DU145 and DU145-FABP5-KO cells. Since neither of the proteins were detectable in either cell line, no quantification was possible. The relative protein levels were reproduced independently three times, and the differences were assessed by Student's t-test. *** P<0.0001 and **** P<0.00001. KO, knockout; FABP5, fatty acid-binding protein 5; AR, androgen receptor; ARFL, full-length AR; ARV7, AR splicing variant 7; PPARγ, peroxisome proliferator-activated receptor-γ; pPPARγ, phosphorylated PPARγ; VEGF, vascular endothelium growth factor; ns, not statistically significant.

Techniques: Invasion Assay, Migration, Western Blot, Knock-Out, Binding Assay, Variant Assay

Effect of FABP5 -KO on malignant characteristics of PC3M and on levels of the downstream proteins of the FABP5 signalling pathway. (A) Microscopical images of PC3M and PC3M-FABP5-KO cells. (B) Proliferation rates of PC3M and PC3M-FABP5-KO cells over the course of the 6-day experimental period. (C) Images of invasive cells from PC3M and PC3M-FABP5-KO at the end of the 6-day experimental period. (D) The average numbers of invasive cells from PC3M and PC3M-FABP5-KO cells. (E) Images of colonies in soft agar formed by PC3M and PC3M-FABP5-KO cells. (F) Average numbers of colonies in soft agar formed by PC3M and PC3M-FABP5-KO cells. (G) Images of wounds in PC3M and PC3M-FABP5-KO cells at the different times. (H) Quantitative assessment of the average size of wound space gap ( μ m) in PC3M and PC3M-FABP5-KO cells. (I) Western blot analysis of PPARγ1 and PPARγ2 in PC3M and PC3M-FABP5-KO cells. (J) Relative levels of PPARγ1 and PPARγ2. Levels of PPARγ1 and PPARγ2 in PC3M were each set at '1', and the levels in PC3M-FABP5-KO cells were obtained by comparing with those in PC3M. (K) Western blots of pPPARγ1 and pPPARγ2 in PC3M and PC3M-FABP5-KO cells. (L) Relative levels of pPPARγ1 and pPPARγ2. Levels of pPPARγ1 and pPPARγ2 in PC3M cells were each set at '1', and the levels in PC3M-FABP5-KO cells were obtained by comparing with those in PC3M. (M) Western blot analysis of VEGF in PC3M and PC3M-FABP5-KO cells was performed. (N) The relative level of VEGF. The level of VEGF in PC3M cells was set at '1', and the level of VEGF in the PC3M-FABP5-KO cells was obtained by comparing with that in the PC3M cells. (O) Western blot analysis of ARFL and ARV7 in the PC3M and PC3M-FABP5-KO cells. Since only ARFL was present, and no ARV7 was detected, no quantification of the data was possible. The relative protein levels were reproduced independently three times, and the differences were assessed by Student's t-test. ** P<0.001, *** P<0.0001 and **** P<0.00001. KO, knockout; FABP5, fatty acid-binding protein 5; AR, androgen receptor; ARFL, full-length AR; ARV7, AR splicing variant 7; PPARγ, peroxisome proliferator-activated receptor-γ; pPPARγ, phosphorylated PPARγ; VEGF, vascular endothelium growth factor; ns, not statistically significant.

Journal: International Journal of Oncology

Article Title: FABP5 can substitute for androgen receptor in malignant progression of prostate cancer cells

doi: 10.3892/ijo.2023.5606

Figure Lengend Snippet: Effect of FABP5 -KO on malignant characteristics of PC3M and on levels of the downstream proteins of the FABP5 signalling pathway. (A) Microscopical images of PC3M and PC3M-FABP5-KO cells. (B) Proliferation rates of PC3M and PC3M-FABP5-KO cells over the course of the 6-day experimental period. (C) Images of invasive cells from PC3M and PC3M-FABP5-KO at the end of the 6-day experimental period. (D) The average numbers of invasive cells from PC3M and PC3M-FABP5-KO cells. (E) Images of colonies in soft agar formed by PC3M and PC3M-FABP5-KO cells. (F) Average numbers of colonies in soft agar formed by PC3M and PC3M-FABP5-KO cells. (G) Images of wounds in PC3M and PC3M-FABP5-KO cells at the different times. (H) Quantitative assessment of the average size of wound space gap ( μ m) in PC3M and PC3M-FABP5-KO cells. (I) Western blot analysis of PPARγ1 and PPARγ2 in PC3M and PC3M-FABP5-KO cells. (J) Relative levels of PPARγ1 and PPARγ2. Levels of PPARγ1 and PPARγ2 in PC3M were each set at '1', and the levels in PC3M-FABP5-KO cells were obtained by comparing with those in PC3M. (K) Western blots of pPPARγ1 and pPPARγ2 in PC3M and PC3M-FABP5-KO cells. (L) Relative levels of pPPARγ1 and pPPARγ2. Levels of pPPARγ1 and pPPARγ2 in PC3M cells were each set at '1', and the levels in PC3M-FABP5-KO cells were obtained by comparing with those in PC3M. (M) Western blot analysis of VEGF in PC3M and PC3M-FABP5-KO cells was performed. (N) The relative level of VEGF. The level of VEGF in PC3M cells was set at '1', and the level of VEGF in the PC3M-FABP5-KO cells was obtained by comparing with that in the PC3M cells. (O) Western blot analysis of ARFL and ARV7 in the PC3M and PC3M-FABP5-KO cells. Since only ARFL was present, and no ARV7 was detected, no quantification of the data was possible. The relative protein levels were reproduced independently three times, and the differences were assessed by Student's t-test. ** P<0.001, *** P<0.0001 and **** P<0.00001. KO, knockout; FABP5, fatty acid-binding protein 5; AR, androgen receptor; ARFL, full-length AR; ARV7, AR splicing variant 7; PPARγ, peroxisome proliferator-activated receptor-γ; pPPARγ, phosphorylated PPARγ; VEGF, vascular endothelium growth factor; ns, not statistically significant.

Techniques: Western Blot, Knock-Out, Binding Assay, Variant Assay

Identification of DEGs between the parental cells and their FABP5 - or AR -KO derivatives and the relevant pathways. (A) Top up (red)- or down (green)-regulated 40 DEGs identified from analysis of the microarray heatmaps of 22RV1 and 22RV1-FABP5-KO cells. Red color represents 'up'. (B) Top 30 pathways associated with DEGs with the 22RV1-FABP5-KO cells were revealed by the enrichment bar chart method. (C) Top up (red)- or down (green)-regulated 40 DEGs from analysis of microarray heatmaps of 22RV1 and 22RV1-AR-KO cells. (D) The top 30 pathways associated with the DEGs in 22RV1-AR-KO cells were identified by the enrichment bar chart method. (E) Top up (red)- or down (green)-regulated 40 DEGs identified by analysis of microarray heatmaps of the DU145 and DU145-FABP5-KO cells. (F) Enrichment bar chart, revealing the top 30 pathways associated with DEGs of DU145-FABP5-KO cells. DEGs, differentially expressed genes; KO, knockout; FABP5, fatty acid-binding protein 5; AR, androgen receptor.

Journal: International Journal of Oncology

Article Title: FABP5 can substitute for androgen receptor in malignant progression of prostate cancer cells

doi: 10.3892/ijo.2023.5606

Figure Lengend Snippet: Identification of DEGs between the parental cells and their FABP5 - or AR -KO derivatives and the relevant pathways. (A) Top up (red)- or down (green)-regulated 40 DEGs identified from analysis of the microarray heatmaps of 22RV1 and 22RV1-FABP5-KO cells. Red color represents 'up'. (B) Top 30 pathways associated with DEGs with the 22RV1-FABP5-KO cells were revealed by the enrichment bar chart method. (C) Top up (red)- or down (green)-regulated 40 DEGs from analysis of microarray heatmaps of 22RV1 and 22RV1-AR-KO cells. (D) The top 30 pathways associated with the DEGs in 22RV1-AR-KO cells were identified by the enrichment bar chart method. (E) Top up (red)- or down (green)-regulated 40 DEGs identified by analysis of microarray heatmaps of the DU145 and DU145-FABP5-KO cells. (F) Enrichment bar chart, revealing the top 30 pathways associated with DEGs of DU145-FABP5-KO cells. DEGs, differentially expressed genes; KO, knockout; FABP5, fatty acid-binding protein 5; AR, androgen receptor.

Techniques: Microarray, Knock-Out, Binding Assay

Identification and verification of the six most prominent DEGs between 22RV1 cells and their FABP5 - or AR -KO derivatives, and between DU145 and DU145-FABP5-KO cells. (A) The top 6 DEGs between 22RV1 and 22RV1-FABP5-KO cells, or between 22RV1 and 22RV1-AR-KO cells (cells are represented by different colors), as identified by heatmap analysis. (B) The top 6 DEGs between DU145 and DU145-FABP5-KO cells identified by heatmap analysis. (C) Western blot verification of the top 3 up- and down-regulated DEGs between 22RV1 and 22RV1-FABP5-KO cells. (D) Relative levels of the top 3 up- and down-regulated DEGs between 22RV1 and 22RV1-FABP5-KO cells. (E) Western blot verification of the top 3 up- and down-regulated DEGs between 22RV1 and 22RV1-AR-KO cells. (F) Relative levels of the top 3 up- and down-regulated DEGs between 22RV1 and 22RV1-AR-KO cells. (G) Western blot verification of the top 3 up- and down-regulated DEGs between DU145 and DU145-FABP5-KO cells. (H) Relative levels of the top 3 up- and down-regulated DEGs between DU145 and DU145-FABP5-KO cells. The relative protein levels were reproduced independently three times, and the differences were assessed by Student's t-test. *** P<0.0001 and **** P<0.00001. DEGs, differentially expressed genes; KO, knockout; FABP5, fatty acid-binding protein 5; AR, androgen receptor; ns, not statistically significant.

Journal: International Journal of Oncology

Article Title: FABP5 can substitute for androgen receptor in malignant progression of prostate cancer cells

doi: 10.3892/ijo.2023.5606

Figure Lengend Snippet: Identification and verification of the six most prominent DEGs between 22RV1 cells and their FABP5 - or AR -KO derivatives, and between DU145 and DU145-FABP5-KO cells. (A) The top 6 DEGs between 22RV1 and 22RV1-FABP5-KO cells, or between 22RV1 and 22RV1-AR-KO cells (cells are represented by different colors), as identified by heatmap analysis. (B) The top 6 DEGs between DU145 and DU145-FABP5-KO cells identified by heatmap analysis. (C) Western blot verification of the top 3 up- and down-regulated DEGs between 22RV1 and 22RV1-FABP5-KO cells. (D) Relative levels of the top 3 up- and down-regulated DEGs between 22RV1 and 22RV1-FABP5-KO cells. (E) Western blot verification of the top 3 up- and down-regulated DEGs between 22RV1 and 22RV1-AR-KO cells. (F) Relative levels of the top 3 up- and down-regulated DEGs between 22RV1 and 22RV1-AR-KO cells. (G) Western blot verification of the top 3 up- and down-regulated DEGs between DU145 and DU145-FABP5-KO cells. (H) Relative levels of the top 3 up- and down-regulated DEGs between DU145 and DU145-FABP5-KO cells. The relative protein levels were reproduced independently three times, and the differences were assessed by Student's t-test. *** P<0.0001 and **** P<0.00001. DEGs, differentially expressed genes; KO, knockout; FABP5, fatty acid-binding protein 5; AR, androgen receptor; ns, not statistically significant.

Techniques: Western Blot, Knock-Out, Binding Assay

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