HY-123356 Search Results


siponimod  (MedChemExpress)
93
MedChemExpress siponimod
<t>Siponimod</t> treatment decreased brain injury volume and brain edema on day 3 after ICH. ICH was induced by injecting collagenase into the left striatum of C57BL/6 mice. (A) Representative brain sections were stained with LFB/CV on day 3. The areas of the lesion lacking staining are circled with a black curve (red arrow indicated); scale bar = 1 mm. (B) Brain injury volume was measured in LFB/CV-stained brain sections. The analysis revealed that siponimod treatment decreased brain injury volume compared to the vehicle-treated group on day 3 post-ICH. The t -test for the analysis of brain injury volume. n = 10 mice per group. (C) On day 3 after ICH, siponimod treatment decreased the water content of the ipsilateral striatum. One-way ANOVA followed by Bonferroni’s post hoc test for the analysis of brain water content. n = 6 mice per group. (D) Siponimod treatment did not influence brain swelling on day 3 after ICH. The t -test for the analysis of brain swelling. n = 10 mice per group. All data are expressed as mean ± SD. Ipsi: ipsilateral, Contra: contralateral.
Siponimod, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/siponimod/product/MedChemExpress
Average 93 stars, based on 1 article reviews
siponimod - by Bioz Stars, 2026-02
93/100 stars
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kmt5a inhibitor unc0379  (MedChemExpress)
92
MedChemExpress kmt5a inhibitor unc0379
<t>KMT5A</t> mediates DTX resistance in BRCA cells. (A) Expression of KMT5A in BRCA. (B) Representative images of immunohistochemical staining of KMT5A in BRCA tumors. (C and D) After 72-h infection, cells were observed, and images were captured by fluorescence microscope. Magnification, ×100. Expression of KMT5A in BRCA cells was detected by reverse transcription-quantitative PCR and western blotting. (E) MTT assay was performed to examine the cell viability and proliferation. (F) The sensitivity of MCF-7 cell line overexpressing KMT5A to DTX was detected by a CCK-8 assay. (G) Effect of KMT5A knockdown and/or DTX on the cell cycle of the MDA-MB-231 cell line. *P<0.05; **P<0.01 and ***P<0.001. KMT5A, lysine methyltransferase 5A; DTX, docetaxel; BRCA, breast cancer; CCK-8, Cell Counting Kit-8; UALCAN, the university of Alabama at Birmingham database; sh, short hairpin; OE, overexpression; NC, negative control.
Kmt5a Inhibitor Unc0379, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/kmt5a inhibitor unc0379/product/MedChemExpress
Average 92 stars, based on 1 article reviews
kmt5a inhibitor unc0379 - by Bioz Stars, 2026-02
92/100 stars
  Buy from Supplier

Image Search Results


Siponimod treatment decreased brain injury volume and brain edema on day 3 after ICH. ICH was induced by injecting collagenase into the left striatum of C57BL/6 mice. (A) Representative brain sections were stained with LFB/CV on day 3. The areas of the lesion lacking staining are circled with a black curve (red arrow indicated); scale bar = 1 mm. (B) Brain injury volume was measured in LFB/CV-stained brain sections. The analysis revealed that siponimod treatment decreased brain injury volume compared to the vehicle-treated group on day 3 post-ICH. The t -test for the analysis of brain injury volume. n = 10 mice per group. (C) On day 3 after ICH, siponimod treatment decreased the water content of the ipsilateral striatum. One-way ANOVA followed by Bonferroni’s post hoc test for the analysis of brain water content. n = 6 mice per group. (D) Siponimod treatment did not influence brain swelling on day 3 after ICH. The t -test for the analysis of brain swelling. n = 10 mice per group. All data are expressed as mean ± SD. Ipsi: ipsilateral, Contra: contralateral.

Journal: Aging and Disease

Article Title: Lymphocyte-Related Immunomodulatory Therapy with Siponimod (BAF-312) Improves Outcomes in Mice with Acute Intracerebral Hemorrhage

doi: 10.14336/AD.2022.1102

Figure Lengend Snippet: Siponimod treatment decreased brain injury volume and brain edema on day 3 after ICH. ICH was induced by injecting collagenase into the left striatum of C57BL/6 mice. (A) Representative brain sections were stained with LFB/CV on day 3. The areas of the lesion lacking staining are circled with a black curve (red arrow indicated); scale bar = 1 mm. (B) Brain injury volume was measured in LFB/CV-stained brain sections. The analysis revealed that siponimod treatment decreased brain injury volume compared to the vehicle-treated group on day 3 post-ICH. The t -test for the analysis of brain injury volume. n = 10 mice per group. (C) On day 3 after ICH, siponimod treatment decreased the water content of the ipsilateral striatum. One-way ANOVA followed by Bonferroni’s post hoc test for the analysis of brain water content. n = 6 mice per group. (D) Siponimod treatment did not influence brain swelling on day 3 after ICH. The t -test for the analysis of brain swelling. n = 10 mice per group. All data are expressed as mean ± SD. Ipsi: ipsilateral, Contra: contralateral.

Article Snippet: Siponimod (BAF-312, MedChemExpress, HY-12335) at a dose of 1 mg/kg dissolved in 5% DMSO with saline was administered intraperitoneally 30 min after surgery and subcutaneously 24 and 48 h after ICH [ , ].

Techniques: Staining

Siponimod treatment reduced the volume of brain lesions, myelin loss, and brain atrophy on day 28 after ICH. (A) The schematic diagram indicated where in the ICH brain for white matter damage measurements. (B) Representative images of brain sections stained with LFB/CV on day 28. The areas of the lesions are circled with the black curve (the red arrow indicated); scale bar = 1 mm. (C) LFB-stained myelin from brain sections in the perihematomal region on day 28. Scale bar = 1 mm. (D). Quantitative analysis of white matter damage. Treatment with siponimod reduced the loss of LFB-stained myelin in the perihematomal region. The t -test for the analysis of white matter damage. n = 12 mice per group. (E-F) Brain lesion volume and atrophy were measured in LFB/CV-stained brain sections. The scattergram shows the quantitative analysis of residual lesion volume (E) and brain atrophy (F). The t -test for the analysis of the volume of residual brain lesion, the Mann-Whitney U test for the analysis of brain atrophy. n = 12 mice per group. Data for brain atrophy are presented as median and IQR; other data are expressed as mean ± SD.

Journal: Aging and Disease

Article Title: Lymphocyte-Related Immunomodulatory Therapy with Siponimod (BAF-312) Improves Outcomes in Mice with Acute Intracerebral Hemorrhage

doi: 10.14336/AD.2022.1102

Figure Lengend Snippet: Siponimod treatment reduced the volume of brain lesions, myelin loss, and brain atrophy on day 28 after ICH. (A) The schematic diagram indicated where in the ICH brain for white matter damage measurements. (B) Representative images of brain sections stained with LFB/CV on day 28. The areas of the lesions are circled with the black curve (the red arrow indicated); scale bar = 1 mm. (C) LFB-stained myelin from brain sections in the perihematomal region on day 28. Scale bar = 1 mm. (D). Quantitative analysis of white matter damage. Treatment with siponimod reduced the loss of LFB-stained myelin in the perihematomal region. The t -test for the analysis of white matter damage. n = 12 mice per group. (E-F) Brain lesion volume and atrophy were measured in LFB/CV-stained brain sections. The scattergram shows the quantitative analysis of residual lesion volume (E) and brain atrophy (F). The t -test for the analysis of the volume of residual brain lesion, the Mann-Whitney U test for the analysis of brain atrophy. n = 12 mice per group. Data for brain atrophy are presented as median and IQR; other data are expressed as mean ± SD.

Article Snippet: Siponimod (BAF-312, MedChemExpress, HY-12335) at a dose of 1 mg/kg dissolved in 5% DMSO with saline was administered intraperitoneally 30 min after surgery and subcutaneously 24 and 48 h after ICH [ , ].

Techniques: Staining, MANN-WHITNEY

Treatment with siponimod improved long-term neurologic deficits after ICH. (A) The corner turn test (CTT) was not significantly different between the siponimod-treated and vehicle-treated groups (F = 0.659, p = 0.628; p > 0.05 at each time point). Repeated measures ANOVA followed by Bonferroni’s post hoc test for the analysis of CTT. n = 12 mice per group. (B) Compared to the vehicle-treated group, siponimod treatment improved neurologic function evaluated with neurological deficit scores (NDS) in mice on days 3, 7, 14, and 28 (Wald χ 2 = 15.597, p < 0.001). Generalized estimation equations (GEEs) for the analysis of the NDS. n = 12 mice per group. (C) Neurological deficit scores for individual tests on days 1, 3, 7, 14, and 28 (generalized estimation equations, n = 12 mice per group). The CTT data are expressed as mean ± SD, and the NDS data are presented as median and IQR.

Journal: Aging and Disease

Article Title: Lymphocyte-Related Immunomodulatory Therapy with Siponimod (BAF-312) Improves Outcomes in Mice with Acute Intracerebral Hemorrhage

doi: 10.14336/AD.2022.1102

Figure Lengend Snippet: Treatment with siponimod improved long-term neurologic deficits after ICH. (A) The corner turn test (CTT) was not significantly different between the siponimod-treated and vehicle-treated groups (F = 0.659, p = 0.628; p > 0.05 at each time point). Repeated measures ANOVA followed by Bonferroni’s post hoc test for the analysis of CTT. n = 12 mice per group. (B) Compared to the vehicle-treated group, siponimod treatment improved neurologic function evaluated with neurological deficit scores (NDS) in mice on days 3, 7, 14, and 28 (Wald χ 2 = 15.597, p < 0.001). Generalized estimation equations (GEEs) for the analysis of the NDS. n = 12 mice per group. (C) Neurological deficit scores for individual tests on days 1, 3, 7, 14, and 28 (generalized estimation equations, n = 12 mice per group). The CTT data are expressed as mean ± SD, and the NDS data are presented as median and IQR.

Article Snippet: Siponimod (BAF-312, MedChemExpress, HY-12335) at a dose of 1 mg/kg dissolved in 5% DMSO with saline was administered intraperitoneally 30 min after surgery and subcutaneously 24 and 48 h after ICH [ , ].

Techniques:

Siponimod treatment reduced neutrophil infiltration and the number of FJB-positive cells but did not influence microglia/macrophage or astrocytic activation on day 3 after ICH. (A) Schematic diagram of the selected fields for quantification of glial fibrillary acid protein (GFAP), ionized calcium-binding protein-1 (Iba-1), myeloperoxidase (MPO), and FJB-positive cells in 3 comparable sections of each mouse. (B-D) Representative images of immunofluorescence staining for Iba-1 (B), GFAP (C), and MPO (D) in the perihematomal region on day 3. The insets show a higher magnificence of immunofluorescence staining positive cells. Scale bar = 50 μm. (E) Representative images of histologic staining of FJB for degenerating cells on day 3. The inset shows the highest magnificence of FJB-positive cells. Scale bar = 50 μm. (F-I) Scattergrams show the quantitative analysis of Iba-1- (F), GFAP- (G), MPO- (H), and FJB- (I) positive cells. The t-test for the analysis of neutrophil infiltration and microglia/macrophage and astrocytic activation, and the Mann-Whitney U test for the analysis of FJB-positive cells. n = 6 mice per group. The data for FJB-positive cells are presented as median and IQR; other data are expressed as mean ± SD. Iba1: ionized calcium-binding adapter molecule 1, GFAP: glial fibrillary acid protein. MPO: myeloperoxidase, FJB: Fluoro-Jade B.

Journal: Aging and Disease

Article Title: Lymphocyte-Related Immunomodulatory Therapy with Siponimod (BAF-312) Improves Outcomes in Mice with Acute Intracerebral Hemorrhage

doi: 10.14336/AD.2022.1102

Figure Lengend Snippet: Siponimod treatment reduced neutrophil infiltration and the number of FJB-positive cells but did not influence microglia/macrophage or astrocytic activation on day 3 after ICH. (A) Schematic diagram of the selected fields for quantification of glial fibrillary acid protein (GFAP), ionized calcium-binding protein-1 (Iba-1), myeloperoxidase (MPO), and FJB-positive cells in 3 comparable sections of each mouse. (B-D) Representative images of immunofluorescence staining for Iba-1 (B), GFAP (C), and MPO (D) in the perihematomal region on day 3. The insets show a higher magnificence of immunofluorescence staining positive cells. Scale bar = 50 μm. (E) Representative images of histologic staining of FJB for degenerating cells on day 3. The inset shows the highest magnificence of FJB-positive cells. Scale bar = 50 μm. (F-I) Scattergrams show the quantitative analysis of Iba-1- (F), GFAP- (G), MPO- (H), and FJB- (I) positive cells. The t-test for the analysis of neutrophil infiltration and microglia/macrophage and astrocytic activation, and the Mann-Whitney U test for the analysis of FJB-positive cells. n = 6 mice per group. The data for FJB-positive cells are presented as median and IQR; other data are expressed as mean ± SD. Iba1: ionized calcium-binding adapter molecule 1, GFAP: glial fibrillary acid protein. MPO: myeloperoxidase, FJB: Fluoro-Jade B.

Article Snippet: Siponimod (BAF-312, MedChemExpress, HY-12335) at a dose of 1 mg/kg dissolved in 5% DMSO with saline was administered intraperitoneally 30 min after surgery and subcutaneously 24 and 48 h after ICH [ , ].

Techniques: Activation Assay, Binding Assay, Immunofluorescence, Staining, MANN-WHITNEY

Siponimod treatment inhibited CD3 + and CD4 + lymphocyte infiltration in the perihematomal regions on day 3 after ICH. (A). The colonization of CD3, CD4, CD8, and DAPI in the perihematomal region on day 3 after collagenase-induced ICH. CD3 immunoreactivity is shown in green; CD4 immunoreactivity is shown in green; CD8 immunoreactivity is shown in red. Sections were stained with DAPI (blue) to label the nuclei. The insets show a higher magnificence of immunoreactive cells in the corresponding merged images. Scale bar = 50 μm. (B-D). Scattergrams show the quantitative analysis of CD3- (B), CD4- (C) and CD8- (D) positive cells. The selected fields in the 3 comparable sections of each mouse detected for lymphocyte infiltration are similar to . Mann-Whitney U test for the analysis of CD3 + and CD8 + lymphocytes, t -test for the analysis of CD4 + lymphocytes. n = 6 mice per group. Data for CD3 + and CD8 + lymphocytes are presented as median and IQR; other data are expressed as mean ± SD. DAPI: 4′, 6-diamidino-2-phenylindole.

Journal: Aging and Disease

Article Title: Lymphocyte-Related Immunomodulatory Therapy with Siponimod (BAF-312) Improves Outcomes in Mice with Acute Intracerebral Hemorrhage

doi: 10.14336/AD.2022.1102

Figure Lengend Snippet: Siponimod treatment inhibited CD3 + and CD4 + lymphocyte infiltration in the perihematomal regions on day 3 after ICH. (A). The colonization of CD3, CD4, CD8, and DAPI in the perihematomal region on day 3 after collagenase-induced ICH. CD3 immunoreactivity is shown in green; CD4 immunoreactivity is shown in green; CD8 immunoreactivity is shown in red. Sections were stained with DAPI (blue) to label the nuclei. The insets show a higher magnificence of immunoreactive cells in the corresponding merged images. Scale bar = 50 μm. (B-D). Scattergrams show the quantitative analysis of CD3- (B), CD4- (C) and CD8- (D) positive cells. The selected fields in the 3 comparable sections of each mouse detected for lymphocyte infiltration are similar to . Mann-Whitney U test for the analysis of CD3 + and CD8 + lymphocytes, t -test for the analysis of CD4 + lymphocytes. n = 6 mice per group. Data for CD3 + and CD8 + lymphocytes are presented as median and IQR; other data are expressed as mean ± SD. DAPI: 4′, 6-diamidino-2-phenylindole.

Article Snippet: Siponimod (BAF-312, MedChemExpress, HY-12335) at a dose of 1 mg/kg dissolved in 5% DMSO with saline was administered intraperitoneally 30 min after surgery and subcutaneously 24 and 48 h after ICH [ , ].

Techniques: Staining, MANN-WHITNEY

Siponimod treatment reduced the number of activated T lymphocytes in the perihematomal regions on day 3 after ICH (immunofluorescence). (A). Colocalization of CD3 and NKp46 and CD3 and CD69 in the perihematomal regions on day 3 after collagenase-induced ICH. CD3 immunoreactivity is shown in green; NKp46 is shown in red; CD69 immunoreactivity is shown in red. Sections were stained with DAPI (blue) to label the nuclei. The insets show a higher magnificence of immunoreactive cells in the corresponding merged images. Scale bar = 100 μm. (B-E). Scattergrams show the quantitative analysis of CD3 + NKp46 + (B), CD3 - NKp46 + (C), CD3 + CD69 + (D) and CD3 - CD69 + (E) cells. The selected fields in the 3 comparable sections of each mouse detected for lymphocyte activation are similar to . t-test for the analysis of CD3 + NKp46 + , CD3 + CD69 + , and CD3 - CD69 + cells, Mann-Whitney U test for the analysis of CD3 - NKp46 + cells. n = 6 mice per group. Data for CD3 - NKp46 + cells are presented as median and IQR; other data are expressed as mean ± SD. DAPI: 4′, 6-diamidino-2-phenylindole.

Journal: Aging and Disease

Article Title: Lymphocyte-Related Immunomodulatory Therapy with Siponimod (BAF-312) Improves Outcomes in Mice with Acute Intracerebral Hemorrhage

doi: 10.14336/AD.2022.1102

Figure Lengend Snippet: Siponimod treatment reduced the number of activated T lymphocytes in the perihematomal regions on day 3 after ICH (immunofluorescence). (A). Colocalization of CD3 and NKp46 and CD3 and CD69 in the perihematomal regions on day 3 after collagenase-induced ICH. CD3 immunoreactivity is shown in green; NKp46 is shown in red; CD69 immunoreactivity is shown in red. Sections were stained with DAPI (blue) to label the nuclei. The insets show a higher magnificence of immunoreactive cells in the corresponding merged images. Scale bar = 100 μm. (B-E). Scattergrams show the quantitative analysis of CD3 + NKp46 + (B), CD3 - NKp46 + (C), CD3 + CD69 + (D) and CD3 - CD69 + (E) cells. The selected fields in the 3 comparable sections of each mouse detected for lymphocyte activation are similar to . t-test for the analysis of CD3 + NKp46 + , CD3 + CD69 + , and CD3 - CD69 + cells, Mann-Whitney U test for the analysis of CD3 - NKp46 + cells. n = 6 mice per group. Data for CD3 - NKp46 + cells are presented as median and IQR; other data are expressed as mean ± SD. DAPI: 4′, 6-diamidino-2-phenylindole.

Article Snippet: Siponimod (BAF-312, MedChemExpress, HY-12335) at a dose of 1 mg/kg dissolved in 5% DMSO with saline was administered intraperitoneally 30 min after surgery and subcutaneously 24 and 48 h after ICH [ , ].

Techniques: Immunofluorescence, Staining, Activation Assay, MANN-WHITNEY

Siponimod treatment inhibited lymphocyte infiltration and alleviated Th cell infiltration and activation in the ICH brain on day 3 after ictus (Flow cytometry analysis). (A) Gating strategies for CD45 + , CD3 + , CD3 + CD4 + , CD3 + CD8 + , CD3 - NKp46 + , CD3 - CD19 + , and CD3 + CD4 + CD69 + cells. (B) Representative flow cytometry plot for CD45 + , CD3 + , CD3 + CD4 + , CD3 + CD8 + , CD3 - NKp46 + , CD3 - CD19 + , and CD3 + CD4 + CD69 + cells in brain samples from vehicle- and siponimod-treated mice on day 3 after ICH. (C) Percentages of lymphocytes, Th cells, CTLs, NK cells, and B lymphocytes and the MFI of CD69 in Th cells in vehicle- and siponimod-treated mice on day 3 after ICH ( t -test, n = 6 mice per group). All data are expressed as mean ± SD.

Journal: Aging and Disease

Article Title: Lymphocyte-Related Immunomodulatory Therapy with Siponimod (BAF-312) Improves Outcomes in Mice with Acute Intracerebral Hemorrhage

doi: 10.14336/AD.2022.1102

Figure Lengend Snippet: Siponimod treatment inhibited lymphocyte infiltration and alleviated Th cell infiltration and activation in the ICH brain on day 3 after ictus (Flow cytometry analysis). (A) Gating strategies for CD45 + , CD3 + , CD3 + CD4 + , CD3 + CD8 + , CD3 - NKp46 + , CD3 - CD19 + , and CD3 + CD4 + CD69 + cells. (B) Representative flow cytometry plot for CD45 + , CD3 + , CD3 + CD4 + , CD3 + CD8 + , CD3 - NKp46 + , CD3 - CD19 + , and CD3 + CD4 + CD69 + cells in brain samples from vehicle- and siponimod-treated mice on day 3 after ICH. (C) Percentages of lymphocytes, Th cells, CTLs, NK cells, and B lymphocytes and the MFI of CD69 in Th cells in vehicle- and siponimod-treated mice on day 3 after ICH ( t -test, n = 6 mice per group). All data are expressed as mean ± SD.

Article Snippet: Siponimod (BAF-312, MedChemExpress, HY-12335) at a dose of 1 mg/kg dissolved in 5% DMSO with saline was administered intraperitoneally 30 min after surgery and subcutaneously 24 and 48 h after ICH [ , ].

Techniques: Activation Assay, Flow Cytometry

Treatment with siponimod decreased the expression of IFN-γ, IL-1β, and XCL1 at 36 h after ICH. (A-B) Representative Western blot bands of proinflammatory factor, HMGB1, IFN-γ, IL-1β, RANTES, and XCL1 were detected by loading brain protein samples from sham-operated and ICH mice treated with vehicle or siponimod, and β-actin was used as the loading control. (C-E) Scattergrams show the quantitative analysis of HMGB1, IFN-γ, IL-1β, RANTES, and XCL1 expression at 36 h after ICH. Densitometric quantification suggested that siponimod administration significantly decreased the levels of IFN-γ, IL-1β (D), and XCL1 (E) levels (one-way ANOVA followed by Bonferroni’s post hoc test, n = 6 mice per group), and siponimod treatment also reduced HMGB1 and RANTES (C) levels. However, it did not reach statistical significance (Kruskal-Wallis test for multiple comparisons, n = 6 mice per group). Data for HMGB1 and RANTES are presented as median and IQR; other data are expressed as mean ± SD. RANTES: On activation, normal T cells were expressed and secreted.

Journal: Aging and Disease

Article Title: Lymphocyte-Related Immunomodulatory Therapy with Siponimod (BAF-312) Improves Outcomes in Mice with Acute Intracerebral Hemorrhage

doi: 10.14336/AD.2022.1102

Figure Lengend Snippet: Treatment with siponimod decreased the expression of IFN-γ, IL-1β, and XCL1 at 36 h after ICH. (A-B) Representative Western blot bands of proinflammatory factor, HMGB1, IFN-γ, IL-1β, RANTES, and XCL1 were detected by loading brain protein samples from sham-operated and ICH mice treated with vehicle or siponimod, and β-actin was used as the loading control. (C-E) Scattergrams show the quantitative analysis of HMGB1, IFN-γ, IL-1β, RANTES, and XCL1 expression at 36 h after ICH. Densitometric quantification suggested that siponimod administration significantly decreased the levels of IFN-γ, IL-1β (D), and XCL1 (E) levels (one-way ANOVA followed by Bonferroni’s post hoc test, n = 6 mice per group), and siponimod treatment also reduced HMGB1 and RANTES (C) levels. However, it did not reach statistical significance (Kruskal-Wallis test for multiple comparisons, n = 6 mice per group). Data for HMGB1 and RANTES are presented as median and IQR; other data are expressed as mean ± SD. RANTES: On activation, normal T cells were expressed and secreted.

Article Snippet: Siponimod (BAF-312, MedChemExpress, HY-12335) at a dose of 1 mg/kg dissolved in 5% DMSO with saline was administered intraperitoneally 30 min after surgery and subcutaneously 24 and 48 h after ICH [ , ].

Techniques: Expressing, Western Blot, Control, Activation Assay

Anti-CD3 Abs alleviated the effects of siponimod on lymphocyte activation and Th1-type cytokine production in the acute phase of ICH. (A) Representative flow cytometry plots of CD3 + , CD3 + CD4 + , CD3 + CD4 - , and CD3 + CD4 + CD69 + cells in the hemorrhagic brain of the ICH + IgG isotype group, the ICH + anti-CD3 Ab group, and the ICH + anti-CD3 Abs + Siponimod group on day 3 after ICH. (B) Percentages of lymphocytes, Th cells, CD3 + CD4 - cells, and MFI of CD69 in Th cells in mice in the three groups on day 3 after ICH (one-way ANOVA followed by Bonferroni’s post hoc test, n = 6 per group). All data are expressed as mean ± SD. (C) Representative Western blot bands of IFN-γ, IL-1β, and XCL1 from mice of the ICH + IgG isotype group, the ICH + anti-CD3 Ab group, the ICH + IgG isotype control + Siponimod group, and the ICH + anti-CD3 Abs + Siponimod group. β-actin was used as a loading control. (D) Quantitative analysis of IFN-γ, IL-1β, and XCL1 expression 36 h after ICH (one-way ANOVA followed by Bonferroni’s post hoc test, n = 6 mice per group). All data are expressed as mean ± SD.

Journal: Aging and Disease

Article Title: Lymphocyte-Related Immunomodulatory Therapy with Siponimod (BAF-312) Improves Outcomes in Mice with Acute Intracerebral Hemorrhage

doi: 10.14336/AD.2022.1102

Figure Lengend Snippet: Anti-CD3 Abs alleviated the effects of siponimod on lymphocyte activation and Th1-type cytokine production in the acute phase of ICH. (A) Representative flow cytometry plots of CD3 + , CD3 + CD4 + , CD3 + CD4 - , and CD3 + CD4 + CD69 + cells in the hemorrhagic brain of the ICH + IgG isotype group, the ICH + anti-CD3 Ab group, and the ICH + anti-CD3 Abs + Siponimod group on day 3 after ICH. (B) Percentages of lymphocytes, Th cells, CD3 + CD4 - cells, and MFI of CD69 in Th cells in mice in the three groups on day 3 after ICH (one-way ANOVA followed by Bonferroni’s post hoc test, n = 6 per group). All data are expressed as mean ± SD. (C) Representative Western blot bands of IFN-γ, IL-1β, and XCL1 from mice of the ICH + IgG isotype group, the ICH + anti-CD3 Ab group, the ICH + IgG isotype control + Siponimod group, and the ICH + anti-CD3 Abs + Siponimod group. β-actin was used as a loading control. (D) Quantitative analysis of IFN-γ, IL-1β, and XCL1 expression 36 h after ICH (one-way ANOVA followed by Bonferroni’s post hoc test, n = 6 mice per group). All data are expressed as mean ± SD.

Article Snippet: Siponimod (BAF-312, MedChemExpress, HY-12335) at a dose of 1 mg/kg dissolved in 5% DMSO with saline was administered intraperitoneally 30 min after surgery and subcutaneously 24 and 48 h after ICH [ , ].

Techniques: Activation Assay, Flow Cytometry, Western Blot, Control, Expressing

KMT5A mediates DTX resistance in BRCA cells. (A) Expression of KMT5A in BRCA. (B) Representative images of immunohistochemical staining of KMT5A in BRCA tumors. (C and D) After 72-h infection, cells were observed, and images were captured by fluorescence microscope. Magnification, ×100. Expression of KMT5A in BRCA cells was detected by reverse transcription-quantitative PCR and western blotting. (E) MTT assay was performed to examine the cell viability and proliferation. (F) The sensitivity of MCF-7 cell line overexpressing KMT5A to DTX was detected by a CCK-8 assay. (G) Effect of KMT5A knockdown and/or DTX on the cell cycle of the MDA-MB-231 cell line. *P<0.05; **P<0.01 and ***P<0.001. KMT5A, lysine methyltransferase 5A; DTX, docetaxel; BRCA, breast cancer; CCK-8, Cell Counting Kit-8; UALCAN, the university of Alabama at Birmingham database; sh, short hairpin; OE, overexpression; NC, negative control.

Journal: Oncology Reports

Article Title: Inhibition of FBP1 expression by KMT5A through TWIST1 methylation is one of the mechanisms leading to chemoresistance in breast cancer

doi: 10.3892/or.2024.8769

Figure Lengend Snippet: KMT5A mediates DTX resistance in BRCA cells. (A) Expression of KMT5A in BRCA. (B) Representative images of immunohistochemical staining of KMT5A in BRCA tumors. (C and D) After 72-h infection, cells were observed, and images were captured by fluorescence microscope. Magnification, ×100. Expression of KMT5A in BRCA cells was detected by reverse transcription-quantitative PCR and western blotting. (E) MTT assay was performed to examine the cell viability and proliferation. (F) The sensitivity of MCF-7 cell line overexpressing KMT5A to DTX was detected by a CCK-8 assay. (G) Effect of KMT5A knockdown and/or DTX on the cell cycle of the MDA-MB-231 cell line. *P<0.05; **P<0.01 and ***P<0.001. KMT5A, lysine methyltransferase 5A; DTX, docetaxel; BRCA, breast cancer; CCK-8, Cell Counting Kit-8; UALCAN, the university of Alabama at Birmingham database; sh, short hairpin; OE, overexpression; NC, negative control.

Article Snippet: BRCA cell lines were treated with KMT5A inhibitor UNC0379 (0, 5 or 10 μM) (MedChemExpress) and DTX (20 μM) for 48 h. A total of 10 μl of diluted CCK-8 was added into each well and cells were incubated in a 5% CO 2 incubator for 2 h at 37°C.

Techniques: Expressing, Immunohistochemical staining, Staining, Infection, Fluorescence, Microscopy, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, MTT Assay, CCK-8 Assay, Knockdown, Cell Counting, Over Expression, Negative Control

FBP1 is upregulated by KMT5A knockdown. (A) Volcano map demonstrating 414 differentially expressed proteins between control (n=3) and KMT5A-knockdown groups (n=3). Red indicates upregulation, and blue indicates deregulation. (B) Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis of 414 target proteins. (C) GO analysis of 414 target proteins. The colors represent GO functional categories (red: Biological Process, green: Molecular Function, blue: Cellular Component). The length of the bar chart to the right of the origin indicates the number of different expressed proteins included in the function. (D) Expression of FBP1 in breast cancer. (E) After 72 h of infection, cells were observed and images were captured by fluorescence microscope. Magnification, ×100. Expression of FBP1 in breast cancer cells was detected by reverse transcription-quantitative PCR and western blotting. (F) The cell cycle analysis of the FBP1-overexpressing group. (G) CCK-8 assay was used to detect the cell viability and proliferation after the addition of docetaxel. *P<0.05, **P<0.01 and ***P<0.001. FBP1, fructose-1,6-bisphosphatase; KMT5A, lysine methyltransferase 5A; GO, Gene Ontology; CCK-8, Cell Counting Kit-8; DTX, docetaxel; UALCAN, the university of Alabama at Birmingham database; HPA, human protein atlas; sh-, short hairpin; NC, negative controls; OE, overexpression; ns, no significance (P≥0.05).

Journal: Oncology Reports

Article Title: Inhibition of FBP1 expression by KMT5A through TWIST1 methylation is one of the mechanisms leading to chemoresistance in breast cancer

doi: 10.3892/or.2024.8769

Figure Lengend Snippet: FBP1 is upregulated by KMT5A knockdown. (A) Volcano map demonstrating 414 differentially expressed proteins between control (n=3) and KMT5A-knockdown groups (n=3). Red indicates upregulation, and blue indicates deregulation. (B) Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis of 414 target proteins. (C) GO analysis of 414 target proteins. The colors represent GO functional categories (red: Biological Process, green: Molecular Function, blue: Cellular Component). The length of the bar chart to the right of the origin indicates the number of different expressed proteins included in the function. (D) Expression of FBP1 in breast cancer. (E) After 72 h of infection, cells were observed and images were captured by fluorescence microscope. Magnification, ×100. Expression of FBP1 in breast cancer cells was detected by reverse transcription-quantitative PCR and western blotting. (F) The cell cycle analysis of the FBP1-overexpressing group. (G) CCK-8 assay was used to detect the cell viability and proliferation after the addition of docetaxel. *P<0.05, **P<0.01 and ***P<0.001. FBP1, fructose-1,6-bisphosphatase; KMT5A, lysine methyltransferase 5A; GO, Gene Ontology; CCK-8, Cell Counting Kit-8; DTX, docetaxel; UALCAN, the university of Alabama at Birmingham database; HPA, human protein atlas; sh-, short hairpin; NC, negative controls; OE, overexpression; ns, no significance (P≥0.05).

Article Snippet: BRCA cell lines were treated with KMT5A inhibitor UNC0379 (0, 5 or 10 μM) (MedChemExpress) and DTX (20 μM) for 48 h. A total of 10 μl of diluted CCK-8 was added into each well and cells were incubated in a 5% CO 2 incubator for 2 h at 37°C.

Techniques: Knockdown, Control, Functional Assay, Expressing, Infection, Fluorescence, Microscopy, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Cell Cycle Assay, CCK-8 Assay, Cell Counting, Over Expression

KMT5A inhibits FBP1 expression. (A) Correlation between the expression of KMT5A and FBP1 based on TCGA cohort [Pearson correlation coefficient (r)=0.131, P<0.05]. (B) The expression of FBP1 was detected by RT-qPCR and western blotting after KMT5A was knocked down. (C) The relationship between KMT5A and FBP1 was verified by dual-luciferase reporter gene assay. (D) The effect of infection of shKMT5A and FBP1 lentivirus in the breast cancer cells were detected by RT-qPCR and western blotting. *P<0.05, **P<0.01 and ***P<0.001. KMT5A, lysine methyltransferase 5A; FBP1, fructose-1,6-bisphosphatase; RT-qPCR, reverse transcription-quantitative PCR; sh-, short hairpin; NC, negative controls; WT, wild-type; RLUC, Renilla luciferase; FLUC, firefly luciferase; Luc, luciferase; OE, overexpression; ns, no significance (P≥0.05).

Journal: Oncology Reports

Article Title: Inhibition of FBP1 expression by KMT5A through TWIST1 methylation is one of the mechanisms leading to chemoresistance in breast cancer

doi: 10.3892/or.2024.8769

Figure Lengend Snippet: KMT5A inhibits FBP1 expression. (A) Correlation between the expression of KMT5A and FBP1 based on TCGA cohort [Pearson correlation coefficient (r)=0.131, P<0.05]. (B) The expression of FBP1 was detected by RT-qPCR and western blotting after KMT5A was knocked down. (C) The relationship between KMT5A and FBP1 was verified by dual-luciferase reporter gene assay. (D) The effect of infection of shKMT5A and FBP1 lentivirus in the breast cancer cells were detected by RT-qPCR and western blotting. *P<0.05, **P<0.01 and ***P<0.001. KMT5A, lysine methyltransferase 5A; FBP1, fructose-1,6-bisphosphatase; RT-qPCR, reverse transcription-quantitative PCR; sh-, short hairpin; NC, negative controls; WT, wild-type; RLUC, Renilla luciferase; FLUC, firefly luciferase; Luc, luciferase; OE, overexpression; ns, no significance (P≥0.05).

Article Snippet: BRCA cell lines were treated with KMT5A inhibitor UNC0379 (0, 5 or 10 μM) (MedChemExpress) and DTX (20 μM) for 48 h. A total of 10 μl of diluted CCK-8 was added into each well and cells were incubated in a 5% CO 2 incubator for 2 h at 37°C.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Luciferase, Reporter Gene Assay, Infection, Reverse Transcription, Real-time Polymerase Chain Reaction, Over Expression

KMT5A relies on methylase activity to inhibit FBP1. (A) KMT5A inhibitor UNC0379 was used to treat breast cancer cells to detect cell activity. (B and C) MDA-MB-231 cells were treated with KMT5A inhibitor UNC0379 to detect lactic acid production and glucose uptake. (D) The effect of KMT5A methylation activity on the FBP1 promoter was detected by dual-luciferase reporter gene assay. KMT5A-R295G is a mutant without methylase activity. (E) The Human Protein Atlas database ( https://www.proteinatlas.org/ ) revealed the interaction networks of KMT5A and TWIST1. (F) Correlation between TWIST1 and FBP1 promoter was detected by dual-luciferase reporter gene assay. ns, P≥0.05; *P<0.05, **P<0.01 and ***P<0.001. KMT5A, lysine methyltransferase 5A; FBP1, fructose-1,6-bisphosphatase; TWIST1, twist family BHLH transcription factor 1; DTX, docetaxel; WT, wild-type; RLUC, Renilla luciferase; FLUC, firefly luciferase; Luc, luciferase; ns, no significance (P≥0.05).

Journal: Oncology Reports

Article Title: Inhibition of FBP1 expression by KMT5A through TWIST1 methylation is one of the mechanisms leading to chemoresistance in breast cancer

doi: 10.3892/or.2024.8769

Figure Lengend Snippet: KMT5A relies on methylase activity to inhibit FBP1. (A) KMT5A inhibitor UNC0379 was used to treat breast cancer cells to detect cell activity. (B and C) MDA-MB-231 cells were treated with KMT5A inhibitor UNC0379 to detect lactic acid production and glucose uptake. (D) The effect of KMT5A methylation activity on the FBP1 promoter was detected by dual-luciferase reporter gene assay. KMT5A-R295G is a mutant without methylase activity. (E) The Human Protein Atlas database ( https://www.proteinatlas.org/ ) revealed the interaction networks of KMT5A and TWIST1. (F) Correlation between TWIST1 and FBP1 promoter was detected by dual-luciferase reporter gene assay. ns, P≥0.05; *P<0.05, **P<0.01 and ***P<0.001. KMT5A, lysine methyltransferase 5A; FBP1, fructose-1,6-bisphosphatase; TWIST1, twist family BHLH transcription factor 1; DTX, docetaxel; WT, wild-type; RLUC, Renilla luciferase; FLUC, firefly luciferase; Luc, luciferase; ns, no significance (P≥0.05).

Article Snippet: BRCA cell lines were treated with KMT5A inhibitor UNC0379 (0, 5 or 10 μM) (MedChemExpress) and DTX (20 μM) for 48 h. A total of 10 μl of diluted CCK-8 was added into each well and cells were incubated in a 5% CO 2 incubator for 2 h at 37°C.

Techniques: Activity Assay, Methylation, Luciferase, Reporter Gene Assay, Mutagenesis

The mechanism by which KMT5A inhibits FBP1 and thus promotes docetaxel resistance in breast cancer. KMT5A, lysine methyltransferase 5A; FBP1, fructose-1,6-bisphosphatase; TWIST1, twist family BHLH transcription factor 1.

Journal: Oncology Reports

Article Title: Inhibition of FBP1 expression by KMT5A through TWIST1 methylation is one of the mechanisms leading to chemoresistance in breast cancer

doi: 10.3892/or.2024.8769

Figure Lengend Snippet: The mechanism by which KMT5A inhibits FBP1 and thus promotes docetaxel resistance in breast cancer. KMT5A, lysine methyltransferase 5A; FBP1, fructose-1,6-bisphosphatase; TWIST1, twist family BHLH transcription factor 1.

Article Snippet: BRCA cell lines were treated with KMT5A inhibitor UNC0379 (0, 5 or 10 μM) (MedChemExpress) and DTX (20 μM) for 48 h. A total of 10 μl of diluted CCK-8 was added into each well and cells were incubated in a 5% CO 2 incubator for 2 h at 37°C.

Techniques: