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mouse monoclonal anti gap43 antibody (Santa Cruz Biotechnology)

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Santa Cruz Biotechnology mouse monoclonal anti gap43 antibody

Immunohistochemical staining for PGP9.5, <t>GAP43</t> and tyrosine hydroxylase (TH) in left ventricular myocardium of WT and Nox2 KO mice with saline or Doxorubicin (Dox) treatment. ( A ) PGP9.5. Bar = 20 μm. ( B ) The graph shows the relative expression of myocardial PGP9.5 in the four groups. Values are presented as means ± S.E.M.; n = 5–6. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. ( C ) GAP43. Bar = 100 μm. ( D ) The graph shows the relative expression of myocardial GAP43 in the four groups. Values are presented as means ± S.E.M.; n = 5–6. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. ( E ) TH. Bar = 20 μm. ( F ) The graph shows the relative expression of myocardial TH in the four groups. Values are presented as means ± S.E.M.; n = 5–7. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. Comparisons among groups were performed by one-way ANOVA followed by a Bonferroni post hoc test for multiple comparisons.

Mouse Monoclonal Anti Gap43 Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 339 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mouse monoclonal anti gap43 antibody - by Bioz Stars, 2026-10

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1) Product Images from "NADPH oxidase 2 mediates cardiac sympathetic denervation and myocyte autophagy, resulting in cardiac atrophy and dysfunction in doxorubicin-induced cardiomyopathy"

Article Title: NADPH oxidase 2 mediates cardiac sympathetic denervation and myocyte autophagy, resulting in cardiac atrophy and dysfunction in doxorubicin-induced cardiomyopathy

Journal: Scientific Reports

doi: 10.1038/s41598-024-57090-2

Immunohistochemical staining for PGP9.5, GAP43 and tyrosine hydroxylase (TH) in left ventricular myocardium of WT and Nox2 KO mice with saline or Doxorubicin (Dox) treatment. ( A ) PGP9.5. Bar = 20 μm. ( B ) The graph shows the relative expression of myocardial PGP9.5 in the four groups. Values are presented as means ± S.E.M.; n = 5–6. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. ( C ) GAP43. Bar = 100 μm. ( D ) The graph shows the relative expression of myocardial GAP43 in the four groups. Values are presented as means ± S.E.M.; n = 5–6. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. ( E ) TH. Bar = 20 μm. ( F ) The graph shows the relative expression of myocardial TH in the four groups. Values are presented as means ± S.E.M.; n = 5–7. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. Comparisons among groups were performed by one-way ANOVA followed by a Bonferroni post hoc test for multiple comparisons.

Figure Legend Snippet: Immunohistochemical staining for PGP9.5, GAP43 and tyrosine hydroxylase (TH) in left ventricular myocardium of WT and Nox2 KO mice with saline or Doxorubicin (Dox) treatment. ( A ) PGP9.5. Bar = 20 μm. ( B ) The graph shows the relative expression of myocardial PGP9.5 in the four groups. Values are presented as means ± S.E.M.; n = 5–6. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. ( C ) GAP43. Bar = 100 μm. ( D ) The graph shows the relative expression of myocardial GAP43 in the four groups. Values are presented as means ± S.E.M.; n = 5–6. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. ( E ) TH. Bar = 20 μm. ( F ) The graph shows the relative expression of myocardial TH in the four groups. Values are presented as means ± S.E.M.; n = 5–7. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. Comparisons among groups were performed by one-way ANOVA followed by a Bonferroni post hoc test for multiple comparisons.

Techniques Used: Immunohistochemical staining, Staining, Saline, Expressing

( A – H ) Changes in myocardial PGP9.5, GAP43, tyrosine hydroxylase (TH) and noradrenaline transporter (NET) proteins in WT saline, WT doxorubicin (Dox) and Nox2 KO Dox groups. ( A , B , E , F ) Representative Western blots of PGP9.5, GAP43, TH and NET proteins, respectively. Equal loading of proteins is illustrated by GAPDH bands. ( C , D , G , H ) The graphs show the relative expression of PGP9.5, GAP43, TH and NET in the three groups, respectively. Values are presented as means ± S.E.M.; n = 5–8. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. ( I , J ) Changes in myocardial cross-sectional area in left ventricular myocardium of WT and Nox2 KO mice with saline or Doxorubicin (Dox) treatment. ( I ) The representative photomicrographs of left ventricular myocardium stained by hematoxylin and eosin. Bar = 20 μm. ( J ) The graph shows the mean myocyte cross-sectional area measured by ImageJ. Values are presented as means ± S.E.M.; n = 5–7. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. Comparisons among groups were performed by one-way ANOVA followed by a Bonferroni post hoc test for multiple comparisons.

Figure Legend Snippet: ( A – H ) Changes in myocardial PGP9.5, GAP43, tyrosine hydroxylase (TH) and noradrenaline transporter (NET) proteins in WT saline, WT doxorubicin (Dox) and Nox2 KO Dox groups. ( A , B , E , F ) Representative Western blots of PGP9.5, GAP43, TH and NET proteins, respectively. Equal loading of proteins is illustrated by GAPDH bands. ( C , D , G , H ) The graphs show the relative expression of PGP9.5, GAP43, TH and NET in the three groups, respectively. Values are presented as means ± S.E.M.; n = 5–8. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. ( I , J ) Changes in myocardial cross-sectional area in left ventricular myocardium of WT and Nox2 KO mice with saline or Doxorubicin (Dox) treatment. ( I ) The representative photomicrographs of left ventricular myocardium stained by hematoxylin and eosin. Bar = 20 μm. ( J ) The graph shows the mean myocyte cross-sectional area measured by ImageJ. Values are presented as means ± S.E.M.; n = 5–7. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. Comparisons among groups were performed by one-way ANOVA followed by a Bonferroni post hoc test for multiple comparisons.

Techniques Used: Saline, Western Blot, Expressing, Staining

Scheme showing that doxorubicin induces NADPH oxidase-derived oxidative stress, resulting in cardiac sympathetic nerve terminal abnormalities as evidenced by the decreases in norepinephrine (NE) histofluorescence and PGP9.5, GAP43, tyrosine hydroxylase (TH) and noradrenaline transporter (NET) protein expression, myocyte autophagy activation and myocyte apoptosis—all of which contribute to cardiac atrophy and failure. NADPH oxidase 2 (Nox2) KO attenuates cardiac sympathetic nerve terminal abnormalities, prevents activation of myocyte autophagy and reduces myocyte apoptosis, thereby improving cardiac atrophy and failure in mice after doxorubicin treatment. These findings suggest that the inhibition of NADPH oxidase, the improvement of cardiac sympathetic nerve terminal innervation and/or the reduction of myocyte autophagy could have beneficial effects in doxorubicin cardiomyopathy and heart failure.

Figure Legend Snippet: Scheme showing that doxorubicin induces NADPH oxidase-derived oxidative stress, resulting in cardiac sympathetic nerve terminal abnormalities as evidenced by the decreases in norepinephrine (NE) histofluorescence and PGP9.5, GAP43, tyrosine hydroxylase (TH) and noradrenaline transporter (NET) protein expression, myocyte autophagy activation and myocyte apoptosis—all of which contribute to cardiac atrophy and failure. NADPH oxidase 2 (Nox2) KO attenuates cardiac sympathetic nerve terminal abnormalities, prevents activation of myocyte autophagy and reduces myocyte apoptosis, thereby improving cardiac atrophy and failure in mice after doxorubicin treatment. These findings suggest that the inhibition of NADPH oxidase, the improvement of cardiac sympathetic nerve terminal innervation and/or the reduction of myocyte autophagy could have beneficial effects in doxorubicin cardiomyopathy and heart failure.

Techniques Used: Derivative Assay, Expressing, Activation Assay, Inhibition

Western Blot:

Article Title: DHHC5 Protein Palmitoylates Flotillin-2 and Is Rapidly Degraded on Induction of Neuronal Differentiation in Cultured Cells
Article Snippet: .. Immunoblotting Whole cell lysates or eluates from neutravidin beads were subjected to SDS-PAGE and transferred to nitrocellulose filters, and immunoblots were performed using the following primary antibodies: mouse monoclonal anti-flotillin-2 (1:5000; BD Transduction Laboratories, catalogue number 610383), rabbit polyclonal anti-Rap2b (1:1000, ProteinTech, 16266–1-AP), rabbit polyclonal anti-calnexin antibody (1:1000, Abcam), anti-DHHC5 polyclonal antibody (1:1000; Sigma-Aldrich HPA014670), mouse monoclonal α-adaptin antibody (1:1000, Abcam), mouse anti-β-actin monoclonal antibody (1:5000, Sigma-Aldrich), and mouse monoclonal anti-GAP-43 (Santa-Cruz, SC-17790). .. Bound antibodies were visualized by chemiluminescence using either or sheep anti-mouse IgG, peroxidase-linked species specific F(ab′) 2 fragment or HRP-linked donkey anti-rabbit IgG (both from GE Healthcare).

Article Title: DHHC5 Protein Palmitoylates Flotillin-2 and Is Rapidly Degraded on Induction of Neuronal Differentiation in Cultured Cells
Article Snippet: .. Whole cell lysates or eluates from neutravidin beads were subjected to SDS-PAGE and transferred to nitrocellulose filters, and immunoblots were performed using the following primary antibodies: mouse monoclonal anti-flotillin-2 (1:5000; BD Transduction Laboratories, catalogue number 610383), rabbit polyclonal anti-Rap2b (1:1000, ProteinTech, 16266–1-AP), rabbit polyclonal anti-calnexin antibody (1:1000, Abcam), anti-DHHC5 polyclonal antibody (1:1000; Sigma-Aldrich HPA014670), mouse monoclonal α-adaptin antibody (1:1000, Abcam), mouse anti-β-actin monoclonal antibody (1:5000, Sigma-Aldrich), and mouse monoclonal anti-GAP-43 (Santa-Cruz, SC-17790). .. Bound antibodies were visualized by chemiluminescence using either or sheep anti-mouse IgG, peroxidase-linked species specific F(ab′) 2 fragment or HRP-linked donkey anti-rabbit IgG (both from GE Healthcare).

SDS Page:

Incubation:

Article Title: Anti-inflammatory and anti-apoptotic effects of (RS)-glucoraphanin bioactivated with myrosinase in murine sub-acute and acute MPTP-induced Parkinson’s disease
Article Snippet: 0968-0896/$ see front matter 2013 Published by Elsevier Ltd. http://dx.doi.org/10.1016/j.bmc.2013.05.065 Abbreviations: GL, glucosinolate; PD, Parkinson’s disease; DAT, dopamine transporter; TH, tyrosine hydroxilase; DA, dopaminergic; IL-1b, interleukin-1beta; SNpc, Substantia Nigra pars compacta; MPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; Myr, myrosinase; ITC, isothiocyanates; IHC, immunohistochemical.. ⇑ Corresponding author.. Tel.

Article Title: Selenium and zinc: Two key players against cadmium-induced neuronal toxicity.
Article Snippet: Cadmium (Cd), a worldwide occupational pollutant, is an extremely toxic heavy metal, capable of damaging several organs, including the brain.. Its toxicity has been related to neurodegenerative diseases such as Alzheimer's and Parkinson's diseases.. The neurotoxic potential of Cd has been attributed to the changes induced in the brain enzyme network involved in counteracting oxidative stress.

Blocking Assay:

Saline:

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Journal: Scientific Reports

Article Title: NADPH oxidase 2 mediates cardiac sympathetic denervation and myocyte autophagy, resulting in cardiac atrophy and dysfunction in doxorubicin-induced cardiomyopathy

doi: 10.1038/s41598-024-57090-2

Figure Lengend Snippet: Immunohistochemical staining for PGP9.5, GAP43 and tyrosine hydroxylase (TH) in left ventricular myocardium of WT and Nox2 KO mice with saline or Doxorubicin (Dox) treatment. ( A ) PGP9.5. Bar = 20 μm. ( B ) The graph shows the relative expression of myocardial PGP9.5 in the four groups. Values are presented as means ± S.E.M.; n = 5–6. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. ( C ) GAP43. Bar = 100 μm. ( D ) The graph shows the relative expression of myocardial GAP43 in the four groups. Values are presented as means ± S.E.M.; n = 5–6. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. ( E ) TH. Bar = 20 μm. ( F ) The graph shows the relative expression of myocardial TH in the four groups. Values are presented as means ± S.E.M.; n = 5–7. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. Comparisons among groups were performed by one-way ANOVA followed by a Bonferroni post hoc test for multiple comparisons.

Article Snippet: The paraffin or frozen myocardial tissue sections were blocked with 10% horse or goat serum in PBS, incubated with goat polyclonal anti-PGP9.5 antibody (Sigma-Aldrich, St. Louis, MO), mouse monoclonal anti-GAP43 antibody (Santa Cruz Biotechnology, Dallas, TX), mouse monoclonal anti-tyrosine hydroxylase antibody (Sigma-Aldrich) or mouse monoclonal anti-LC3β antibody (Santa Cruz Biotechnology) and then incubated with biotin-conjugated anti-goat or anti-mouse IgG (Vector Laboratory, Burlingame, CA).

Techniques: Immunohistochemical staining, Staining, Saline, Expressing

Journal: Scientific Reports

Article Title: NADPH oxidase 2 mediates cardiac sympathetic denervation and myocyte autophagy, resulting in cardiac atrophy and dysfunction in doxorubicin-induced cardiomyopathy

doi: 10.1038/s41598-024-57090-2

Figure Lengend Snippet: ( A – H ) Changes in myocardial PGP9.5, GAP43, tyrosine hydroxylase (TH) and noradrenaline transporter (NET) proteins in WT saline, WT doxorubicin (Dox) and Nox2 KO Dox groups. ( A , B , E , F ) Representative Western blots of PGP9.5, GAP43, TH and NET proteins, respectively. Equal loading of proteins is illustrated by GAPDH bands. ( C , D , G , H ) The graphs show the relative expression of PGP9.5, GAP43, TH and NET in the three groups, respectively. Values are presented as means ± S.E.M.; n = 5–8. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. ( I , J ) Changes in myocardial cross-sectional area in left ventricular myocardium of WT and Nox2 KO mice with saline or Doxorubicin (Dox) treatment. ( I ) The representative photomicrographs of left ventricular myocardium stained by hematoxylin and eosin. Bar = 20 μm. ( J ) The graph shows the mean myocyte cross-sectional area measured by ImageJ. Values are presented as means ± S.E.M.; n = 5–7. * P < 0.05 versus WT saline group. # P < 0.05 versus WT Dox group. Comparisons among groups were performed by one-way ANOVA followed by a Bonferroni post hoc test for multiple comparisons.

Techniques: Saline, Western Blot, Expressing, Staining

Journal: Scientific Reports

Article Title: NADPH oxidase 2 mediates cardiac sympathetic denervation and myocyte autophagy, resulting in cardiac atrophy and dysfunction in doxorubicin-induced cardiomyopathy

doi: 10.1038/s41598-024-57090-2

Figure Lengend Snippet: Scheme showing that doxorubicin induces NADPH oxidase-derived oxidative stress, resulting in cardiac sympathetic nerve terminal abnormalities as evidenced by the decreases in norepinephrine (NE) histofluorescence and PGP9.5, GAP43, tyrosine hydroxylase (TH) and noradrenaline transporter (NET) protein expression, myocyte autophagy activation and myocyte apoptosis—all of which contribute to cardiac atrophy and failure. NADPH oxidase 2 (Nox2) KO attenuates cardiac sympathetic nerve terminal abnormalities, prevents activation of myocyte autophagy and reduces myocyte apoptosis, thereby improving cardiac atrophy and failure in mice after doxorubicin treatment. These findings suggest that the inhibition of NADPH oxidase, the improvement of cardiac sympathetic nerve terminal innervation and/or the reduction of myocyte autophagy could have beneficial effects in doxorubicin cardiomyopathy and heart failure.

Techniques: Derivative Assay, Expressing, Activation Assay, Inhibition

Callosal axonal projections. (A) Scheme of a frontal section of the brain from a normal mouse embryo at E16.5 representing the populations implicated in the correct corpus callosum development. (B) DiI-tracing experiment to label the callosal fibers in fixed mouse brains at P1. The positions where the DiI crystals were placed are shown (asterisks). The callosal fibers can be detected crossing the midline in the wild-type (wt) mouse (Top). However, in the hyh mutant mouse (Bottom), callosal axons do not cross the midline and form Probst Bundles (PB). Schemes on the right depict where DiI crystals were placed and the path that callosal axons follow. (C) Frontal sections of wt (Left) and hyh (Right) mutant mice brain at E15.5 showing GAP-43 immunostaining. The main anatomical structures detected in the pictures are depicted in schemes on the bottom. In wt and hyh mutant mice, pioneering axons are GAP43-positive (arrows) and do not show any anatomical alteration in the hyh mouse. (D) Frontal sections of mice brains at P1 showing NCAM immunolabeling. In wt (Top) and hyh mutant (Bottom) mice, callosal axons are NCAM positive (arrows). Frames 1 and 2 are shown in detail. AC, Anterior Commissure; CC, Corpus Callosum; CgC, Cingulate Cortex; IF, Interhemispheric Fissure; LV, Lateral Ventricle; cLV, collapsed Lateral Ventricle. Scale Bars: (B) , 200 μm; (C) , 100 μm; (D) , Panoramic, 100 μm; Frame 1 and Frame 2, 50 μm.

Journal: Frontiers in Cellular Neuroscience

Article Title: A selective defect in the glial wedge as part of the neuroepithelium disruption in hydrocephalus development in the mouse hyh model is associated with complete corpus callosum dysgenesis

doi: 10.3389/fncel.2024.1330412

Figure Lengend Snippet: Callosal axonal projections. (A) Scheme of a frontal section of the brain from a normal mouse embryo at E16.5 representing the populations implicated in the correct corpus callosum development. (B) DiI-tracing experiment to label the callosal fibers in fixed mouse brains at P1. The positions where the DiI crystals were placed are shown (asterisks). The callosal fibers can be detected crossing the midline in the wild-type (wt) mouse (Top). However, in the hyh mutant mouse (Bottom), callosal axons do not cross the midline and form Probst Bundles (PB). Schemes on the right depict where DiI crystals were placed and the path that callosal axons follow. (C) Frontal sections of wt (Left) and hyh (Right) mutant mice brain at E15.5 showing GAP-43 immunostaining. The main anatomical structures detected in the pictures are depicted in schemes on the bottom. In wt and hyh mutant mice, pioneering axons are GAP43-positive (arrows) and do not show any anatomical alteration in the hyh mouse. (D) Frontal sections of mice brains at P1 showing NCAM immunolabeling. In wt (Top) and hyh mutant (Bottom) mice, callosal axons are NCAM positive (arrows). Frames 1 and 2 are shown in detail. AC, Anterior Commissure; CC, Corpus Callosum; CgC, Cingulate Cortex; IF, Interhemispheric Fissure; LV, Lateral Ventricle; cLV, collapsed Lateral Ventricle. Scale Bars: (B) , 200 μm; (C) , 100 μm; (D) , Panoramic, 100 μm; Frame 1 and Frame 2, 50 μm.

Article Snippet: WI, USA); mouse monoclonal anti-GAP-43 (1:2000 dilution, G9264, Clone GAP-7B10, Sigma-Aldrich, St. Louis, MO, USA); rabbit polyclonal anti-GFAP (1:1000 dilution, Z0334, Agilent Dako, Santa Clara, CA, USA); mouse monoclonal anti-GFAP (1:1000 dilution, G-A-5, Sigma-Aldrich, St. Louis, MO, USA); mouse monoclonal anti-NCAM (undiluted, 5B8 clone, Developmental Studies Hybridoma Bank, DSHB, Iowa City, IA); rabbit monoclonal anti-NeuN (1:500 dilution, ab177487, Abcam, Cambridge, UK); mouse monoclonal anti-Nestin (1:200 dilution, clone Rat-401, DSHB); mouse monoclonal anti-PCNA (1:200 dilution, MAB424, Clone PC10, Sigma-Aldrich, St. Louis, MO, USA); and rabbit monoclonal anti-Slit2 (1:500 dilution, ab134166 Abcam, Cambridge, UK).

Techniques: Mutagenesis, Immunostaining, Immunolabeling

Localisation and mean density of BrdU (A–C), Ki67 (D–F), cleaved caspase 3 (G–I), GAP 43 (J–L), doublecortin (M–O) and OMP (P–R) labelled cells in the olfactory epithelium of WT and STOP null mice. The x-axis refers to the six levels studied, from rostral (level 1) to caudal (level 6). A statistically significant increase in the number of proliferating (BrdU and Ki67 positive cells), apoptotic (caspase 3 positive cells) and immature neurons (GAP 43 and doublecortin positive cells) was observed in STOP null mice as compared to WT mice. There was no difference in the number of mature OMP expressing neurons between the two genotypes. All values are represented as mean +/− SEM, *p<0.05, **p<0.01. Scale bar: 25 µm.

Journal: PLoS ONE

Article Title: Loss of STOP Protein Impairs Peripheral Olfactory Neurogenesis

doi: 10.1371/journal.pone.0012753

Figure Lengend Snippet: Localisation and mean density of BrdU (A–C), Ki67 (D–F), cleaved caspase 3 (G–I), GAP 43 (J–L), doublecortin (M–O) and OMP (P–R) labelled cells in the olfactory epithelium of WT and STOP null mice. The x-axis refers to the six levels studied, from rostral (level 1) to caudal (level 6). A statistically significant increase in the number of proliferating (BrdU and Ki67 positive cells), apoptotic (caspase 3 positive cells) and immature neurons (GAP 43 and doublecortin positive cells) was observed in STOP null mice as compared to WT mice. There was no difference in the number of mature OMP expressing neurons between the two genotypes. All values are represented as mean +/− SEM, *p<0.05, **p<0.01. Scale bar: 25 µm.

Article Snippet: The following antibodies were used: polyclonal rabbit anti-STOP protein , anti-GAP 43 (for the analyses of immature cells in the OE and VNE; 1∶5000, Chemicon, Abcys, Paris, France), anti-cleaved caspase 3 (1∶1000, Cell Signalling, Abcam, Cambrige, UK), anti-doublecortin (1∶5000, Abcam, Cambridge, UK), anti-cytokeratin 5 (1∶5000, Abcam, Cambridge, UK), anti-Vglut2 (Synaptic Systems, Gottingen, Germany), goat polyclonal anti-OMP (1∶5000, Wako Chemicals, Neuss, Germany), mouse monoclonal anti-GAP 43 (for the analysis in the OB; 1∶5000, Sigma, Saint-Quentin Fallavier, France), rat monoclonal anti-BrdU (1∶1000, Abcam, Cambridge, UK), rabbit monoclonal anti-Ki67 (1∶500, Microm Microtech, Francheville, France).

Techniques: Expressing

Localisation and mean density of BrdU (A–C), Ki67 (D–F), cleaved caspase 3 (G–I), GAP 43 (J–L), doublecortin (M–O) and OMP (P–R) labelled cells in the vomeronasal epithelium of WT and STOP null mice. The x-axis refers to the three levels studied, from rostral (level 1) to caudal (level 3), where the vomeronasal organ was present. A statistically significant increase in proliferating (BrdU and Ki67 positive cells), apoptotic (caspase 3 positive cells) and immature neurons (GAP 43 and doublecortin positive cells), but not mature OMP positive neurons was observed in STOP null mice as compared to WT mice. All values are represented as mean +/− SEM, *p<0.05, **p<0.01. Scale bar: 100 µm.

Journal: PLoS ONE

Article Title: Loss of STOP Protein Impairs Peripheral Olfactory Neurogenesis

doi: 10.1371/journal.pone.0012753

Figure Lengend Snippet: Localisation and mean density of BrdU (A–C), Ki67 (D–F), cleaved caspase 3 (G–I), GAP 43 (J–L), doublecortin (M–O) and OMP (P–R) labelled cells in the vomeronasal epithelium of WT and STOP null mice. The x-axis refers to the three levels studied, from rostral (level 1) to caudal (level 3), where the vomeronasal organ was present. A statistically significant increase in proliferating (BrdU and Ki67 positive cells), apoptotic (caspase 3 positive cells) and immature neurons (GAP 43 and doublecortin positive cells), but not mature OMP positive neurons was observed in STOP null mice as compared to WT mice. All values are represented as mean +/− SEM, *p<0.05, **p<0.01. Scale bar: 100 µm.

Techniques:

Mean density of Ki 67 (A, B), caspase 3 (C, D), GAP 43 (E, F) and OMP (G, H) positive cells in the olfactory epithelium of WT and STOP null mice at two different ages. In the 3-month-old groups (A, C, E, G), apoptotic, proliferating and immature, but not mature neurons are more numerous in STOP null mice as compared to WT mice, both in control animals and after regeneration. In the 10-month-old groups (B, D, F, H) only the number of caspase 3 positive neurons (D) was increased in STOP null mice as compared to WT mice, in controls and after regeneration. All values are represented as mean +/− SEM, *p<0.05, **p<0.01. The photomicrographs illustrate immunostaining in animals after regeneration. Scale bar: 25 µm.

Journal: PLoS ONE

Article Title: Loss of STOP Protein Impairs Peripheral Olfactory Neurogenesis

doi: 10.1371/journal.pone.0012753

Figure Lengend Snippet: Mean density of Ki 67 (A, B), caspase 3 (C, D), GAP 43 (E, F) and OMP (G, H) positive cells in the olfactory epithelium of WT and STOP null mice at two different ages. In the 3-month-old groups (A, C, E, G), apoptotic, proliferating and immature, but not mature neurons are more numerous in STOP null mice as compared to WT mice, both in control animals and after regeneration. In the 10-month-old groups (B, D, F, H) only the number of caspase 3 positive neurons (D) was increased in STOP null mice as compared to WT mice, in controls and after regeneration. All values are represented as mean +/− SEM, *p<0.05, **p<0.01. The photomicrographs illustrate immunostaining in animals after regeneration. Scale bar: 25 µm.

Techniques: Immunostaining

Mean percentage of OMP (A, B), Vglut2 (C, D), GAP 43 (E, F) positive glomerular areas and mean percentage of caspase 3 (G, H) positive glomeruli in WT and STOP null mice at two different ages. In control groups and after regeneration there was no difference between the two genotypes concerning OMP, Vglut2 and GAP 43 immunolabelling at both ages. In controls and after regeneration, the number of glomeruli with apoptotic fibers was greater in STOP null mice as compared to WT mice at both ages. All values are represented as mean +/− SEM, *p<0.05, **p<0.01. The photomicrographs illustrate immunostaining in animals after regeneration. Scale bar: 25 µm.

Journal: PLoS ONE

Article Title: Loss of STOP Protein Impairs Peripheral Olfactory Neurogenesis

doi: 10.1371/journal.pone.0012753

Figure Lengend Snippet: Mean percentage of OMP (A, B), Vglut2 (C, D), GAP 43 (E, F) positive glomerular areas and mean percentage of caspase 3 (G, H) positive glomeruli in WT and STOP null mice at two different ages. In control groups and after regeneration there was no difference between the two genotypes concerning OMP, Vglut2 and GAP 43 immunolabelling at both ages. In controls and after regeneration, the number of glomeruli with apoptotic fibers was greater in STOP null mice as compared to WT mice at both ages. All values are represented as mean +/− SEM, *p<0.05, **p<0.01. The photomicrographs illustrate immunostaining in animals after regeneration. Scale bar: 25 µm.

Techniques: Immunostaining

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mouse monoclonal anti gap43 antibody (Santa Cruz Biotechnology)

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1) Product Images from "NADPH oxidase 2 mediates cardiac sympathetic denervation and myocyte autophagy, resulting in cardiac atrophy and dysfunction in doxorubicin-induced cardiomyopathy"

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