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slc7a5 mouse monoclonal (Proteintech)

Name: slc7a5 mouse monoclonal
Brand: Proteintech
Rating: 95 (83 reviews)

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Proteintech slc7a5 mouse monoclonal

Slc7a5 Mouse Monoclonal, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 95 stars, based on 1 article reviews

slc7a5 mouse monoclonal - by Bioz Stars, 2025-05

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1) Product Images from "Snapshot of in-cell protein contact sites reveals new host factors and hijacking of paraspeckles during influenza A virus infection"

Article Title: Snapshot of in-cell protein contact sites reveals new host factors and hijacking of paraspeckles during influenza A virus infection

Journal: bioRxiv

doi: 10.1101/2025.03.09.642134

Figure Legend Snippet: (A) Cross-linking network of M2 and LAT1 (B) Log(RLU) normalised to siNT. Data are represented as mean ± SD (n = 3), with individual experiment means shown as circles. Statistical analysis was performed using ordinary one-way ANOVA. Statistical significance: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001. siSLC3A2 is replicated from . (C) Volcano plots showing fold-change (log2) versus significance (-log10 p-value) for SLC7A5 versus isotype control. Viral proteins are depicted in orange, SLC7A5 and SLC3A2 – in green. (D) Maximum intensity projection (MaxIP) of confocal images from A549 cells infected with WSN (Multiplicity of infection (MOI) 3) or mock at 12 hpi. Cells were stained for SLC7A5 (green), M2 (magenta), and nuclei (DAPI, cyan). Scale bars, 20 µm. (E) Pearson’s correlation coefficient quantification of SLC7A5 and M2 colocalisation in membrane regions. Analysis was performed in mock-infected cells (n = 64) and WSN-infected cells at 12 hpi (n = 119). Statistical significance was determined using the Mann-Whitney test (****p<0.0001). (F) Representative plane and intensity profile showing the co-localisation of SLC7A5 and M2 in A549 cells at 12 hpi.

Techniques Used: Control, Infection, Staining, Membrane, MANN-WHITNEY

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Decreased function of NK cells in obese mice upon acute retrovirus infection For 13 weeks, C57BL/6 mice were fed with HFD or CD. At week 12, mice were infected i.v. with FV for 7 days or used as uninfected, naive control. Splenic NK cells (NK1.1 + CD3 − ) were analyzed as percentage (A) or absolute cell numbers (B). NK cells of naive mice are shown in gray, whereas NK cells from FV-infected mice are displayed in white. Statistically significant differences were analyzed by an unpaired t test. Data are presented as mean values ± SEM. FSC-A of NK cells from lean and obese mice are shown in (C). Heat maps show fold changes of percentages (D) and median fluorescence intensity (MFI) (E) of NK cells from naive or FV-infected mice fed with HFD relative to CD (HFD rel. to CD). Eight mice per group from two independent experiments were analyzed by an unpaired t test (KLRG1, CD98, IFNγ, GzmB %, MitoSpy, and puromycin) and Mann-Whitney test (GzmA and GzmB MFI). Statistically significant differences ( p ≤ 0.05) are indicated in the figure. See also <xref ref-type=

Figure S3 . " width="100%" height="100%">

Journal: iScience

Article Title: Dietary lipid overload creates a suppressive environment that impedes the antiviral functions of NK cells

doi: 10.1016/j.isci.2025.112396

Figure Lengend Snippet: Decreased function of NK cells in obese mice upon acute retrovirus infection For 13 weeks, C57BL/6 mice were fed with HFD or CD. At week 12, mice were infected i.v. with FV for 7 days or used as uninfected, naive control. Splenic NK cells (NK1.1 + CD3 − ) were analyzed as percentage (A) or absolute cell numbers (B). NK cells of naive mice are shown in gray, whereas NK cells from FV-infected mice are displayed in white. Statistically significant differences were analyzed by an unpaired t test. Data are presented as mean values ± SEM. FSC-A of NK cells from lean and obese mice are shown in (C). Heat maps show fold changes of percentages (D) and median fluorescence intensity (MFI) (E) of NK cells from naive or FV-infected mice fed with HFD relative to CD (HFD rel. to CD). Eight mice per group from two independent experiments were analyzed by an unpaired t test (KLRG1, CD98, IFNγ, GzmB %, MitoSpy, and puromycin) and Mann-Whitney test (GzmA and GzmB MFI). Statistically significant differences ( p ≤ 0.05) are indicated in the figure. See also Figure S3 .

Article Snippet: Rat monoclonal anti mouse CD98 (4F2) (clone RL388) , BioLegend , Cat# 128216; RRID: AB_2750549.

Techniques: Infection, Control, Fluorescence, MANN-WHITNEY

Tregs negatively regulate NK cells after short-term HFD upon acute retrovirus infection DEREG mice were fed with HFD for a total of 10 days. After 4 days, mice were infected with FV for seven days and depleted for Tregs by i.p. injections of DT (A). mRNA of splenocytes was isolated and analyzed for Il10 expression (B). Seven mice from two independent experiments were used for analyses. Spleen weight (C) and viral loads (D) were determined at 7 dpi (HFD 10 mice, HFD+DT 7 mice). NK cell numbers and percentages are displayed in (E). Proliferation was measured using KI67 (F). Expression of KLRG1 by NK cells is shown in (G). Percentages of degranulating CD107a + NK cells are shown in (H). NK cell cytotoxic capacity was determined by GzmB (I; MFI). Expression levels (MFI) of CD98 (J), MitoSpy (K), and Puromycin (L) in NK cells were analyzed from seven animals of two independent experiments. NK cells were isolated using magnetic beads and co-cultured with CFSE-stained YAC-1 tumor cells. In vitro killing was detected with BD Canto II (M). Five mice (HFD) and 7 mice (HFD+DT) from two independent experiments were used to analyze differences between groups. Statistically significant differences were analysed by an unpaired t test (B, C, F–I, K, and M) or Mann-Whitney test (D). IL-10 was neutralized by repetitive injections of anti-IL-10 monoclonal antibodies in short-term HFD mice (N). Splenic NK cells were isolated with magnetic beads and co-cultured with CFSE-stained YAC-1 tumor cells. In vitro killing was detected with BD Canto II. Nine mice per group from two independent experiments were used and analyzed by an unpaired t test. One outlier was removed (ROUT method). The significance threshold was set at 0.05. Data are presented as mean values ± SEM. DT: diphtheria toxin.

Journal: iScience

Article Title: Dietary lipid overload creates a suppressive environment that impedes the antiviral functions of NK cells

doi: 10.1016/j.isci.2025.112396

Figure Lengend Snippet: Tregs negatively regulate NK cells after short-term HFD upon acute retrovirus infection DEREG mice were fed with HFD for a total of 10 days. After 4 days, mice were infected with FV for seven days and depleted for Tregs by i.p. injections of DT (A). mRNA of splenocytes was isolated and analyzed for Il10 expression (B). Seven mice from two independent experiments were used for analyses. Spleen weight (C) and viral loads (D) were determined at 7 dpi (HFD 10 mice, HFD+DT 7 mice). NK cell numbers and percentages are displayed in (E). Proliferation was measured using KI67 (F). Expression of KLRG1 by NK cells is shown in (G). Percentages of degranulating CD107a + NK cells are shown in (H). NK cell cytotoxic capacity was determined by GzmB (I; MFI). Expression levels (MFI) of CD98 (J), MitoSpy (K), and Puromycin (L) in NK cells were analyzed from seven animals of two independent experiments. NK cells were isolated using magnetic beads and co-cultured with CFSE-stained YAC-1 tumor cells. In vitro killing was detected with BD Canto II (M). Five mice (HFD) and 7 mice (HFD+DT) from two independent experiments were used to analyze differences between groups. Statistically significant differences were analysed by an unpaired t test (B, C, F–I, K, and M) or Mann-Whitney test (D). IL-10 was neutralized by repetitive injections of anti-IL-10 monoclonal antibodies in short-term HFD mice (N). Splenic NK cells were isolated with magnetic beads and co-cultured with CFSE-stained YAC-1 tumor cells. In vitro killing was detected with BD Canto II. Nine mice per group from two independent experiments were used and analyzed by an unpaired t test. One outlier was removed (ROUT method). The significance threshold was set at 0.05. Data are presented as mean values ± SEM. DT: diphtheria toxin.

Article Snippet: Rat monoclonal anti mouse CD98 (4F2) (clone RL388) , BioLegend , Cat# 128216; RRID: AB_2750549.

Techniques: Infection, Isolation, Expressing, Magnetic Beads, Cell Culture, Staining, In Vitro, MANN-WHITNEY, Bioprocessing

Journal: bioRxiv

Article Title: Snapshot of in-cell protein contact sites reveals new host factors and hijacking of paraspeckles during influenza A virus infection

doi: 10.1101/2025.03.09.642134

Figure Lengend Snippet: (A) Cross-linking network of M2 and LAT1 (B) Log(RLU) normalised to siNT. Data are represented as mean ± SD (n = 3), with individual experiment means shown as circles. Statistical analysis was performed using ordinary one-way ANOVA. Statistical significance: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001. siSLC3A2 is replicated from . (C) Volcano plots showing fold-change (log2) versus significance (-log10 p-value) for SLC7A5 versus isotype control. Viral proteins are depicted in orange, SLC7A5 and SLC3A2 – in green. (D) Maximum intensity projection (MaxIP) of confocal images from A549 cells infected with WSN (Multiplicity of infection (MOI) 3) or mock at 12 hpi. Cells were stained for SLC7A5 (green), M2 (magenta), and nuclei (DAPI, cyan). Scale bars, 20 µm. (E) Pearson’s correlation coefficient quantification of SLC7A5 and M2 colocalisation in membrane regions. Analysis was performed in mock-infected cells (n = 64) and WSN-infected cells at 12 hpi (n = 119). Statistical significance was determined using the Mann-Whitney test (****p<0.0001). (F) Representative plane and intensity profile showing the co-localisation of SLC7A5 and M2 in A549 cells at 12 hpi.

Article Snippet: The following primary antibodies were used for western blot analysis: NONO mouse monoclonal (1:1,000, Proteintech, clone 2A2B10, catalogue no. 66361-1-Ig); NONO rabbit polyclonal (1:1,000, Proteintech, catalogue no. 11058-1-AP); SFPQ mouse monoclonal (1:1,000, Proteintech, clone 1G4A5, catalogue no. 67129-1-Ig); SFPQ rabbit polyclonal (1:1,000, Proteintech, catalogue no. 15585-1-AP); PSPC1 rabbit polyclonal (1:1,000, Proteintech, catalogue no. 16714-1-AP); SLC7A5 rabbit polyclonal (1:1,000, Proteintech, catalogue no. 28670-1-AP); SLC7A5 mouse monoclonal (1:1,000, Proteintech, clone 2G5H3, catalogue no. 67951-1-Ig); SLC3A2 rabbit polyclonal (1:1,000, Proteintech, catalogue no 15193-1-AP); SLC3A2 mouse monoclonal (1:1,000, Proteintech, clone 2B10F5, catalogue no. 66883-1-Ig); NP mouse monoclonal (1:1,000, Abcam, clone C43, catalogue no. ab128193); M2 mouse (1:1,000, ThermoFisher, clone 14C2, catalogue no. MA1-082); PB1, PB2, M1 (1: 1000, Abcam ab22396), NS1 (1:1,000, ThermoFisher, MA5-35909); Vinculin mouse (1:5000, Merck, catalogue no. V9131); Cyclophilin B rabbit monoclonal (1:5,000, CST, clone D1V5J, catalogue no. 43603).

Techniques: Control, Infection, Staining, Membrane, MANN-WHITNEY

Journal: bioRxiv

Article Title: Snapshot of in-cell protein contact sites reveals new host factors and hijacking of paraspeckles during influenza A virus infection

doi: 10.1101/2025.03.09.642134

Techniques: Control, Infection, Staining, Membrane, MANN-WHITNEY

Recovery of the KRmem-expressing MRV. The BHK/T7-9 cells in a 6-well plate were transfected with 10 genome plasmids, including the recombinant S2 segment plasmid. Using the fluorescence microscope with the EVOS Light Cube for Texas Red, images were captured throughout a well and were combined using the tiling method. ( A ) The parts of the combined images at 6 and 9 days post transfection are shown. ( B ) The supernatant of the transfected cells was inoculated to BHK/T7-9 cells, and the fluorescence images of the KRmem expression were captured using the light cube for Texas Red. The fluorescent and merged images obtained at 3 and 5 days post infection are shown in pseudo-color.

Journal: Pharmaceuticals

Article Title: Cytocidal Effect of Irradiation on Gastric Cancer Cells Infected with a Recombinant Mammalian Orthoreovirus Expressing a Membrane-Targeted KillerRed

doi: 10.3390/ph17010079

Figure Lengend Snippet: Recovery of the KRmem-expressing MRV. The BHK/T7-9 cells in a 6-well plate were transfected with 10 genome plasmids, including the recombinant S2 segment plasmid. Using the fluorescence microscope with the EVOS Light Cube for Texas Red, images were captured throughout a well and were combined using the tiling method. ( A ) The parts of the combined images at 6 and 9 days post transfection are shown. ( B ) The supernatant of the transfected cells was inoculated to BHK/T7-9 cells, and the fluorescence images of the KRmem expression were captured using the light cube for Texas Red. The fluorescent and merged images obtained at 3 and 5 days post infection are shown in pseudo-color.

Article Snippet: The membrane was blocked with phosphate-buffered saline containing 5% ( w / v ) skim milk and 0.1% ( v / v ) Tween-20, and it was incubated with mouse anti-σ3 mAb (clone 4F2, Developmental Studies Hybridoma Bank), mouse anti-β-actin mAb (clone G043, Applied Biological Materials, Vancouver, BC, Canada), or rabbit anti-KillerRed polyclonal antibody (Evrogen, Moscow, Russia).

Techniques: Expressing, Transfection, Recombinant, Plasmid Preparation, Fluorescence, Microscopy, Infection

Properties of the KRmem-expressing MRV. ( A ) Electrophoretic patterns of genomic dsRNAs extracted from the wild type (WT) or KRmem-expressing virus, T3D-L(S2/3′KRmem). The name of each segment is also indicated. ( B ) Immunofluorescence assay of infected cells. Each virus was inoculated to BHK/T7-9 cells at a multiplicity of infection (MOI) of 100, and cells were fixed and stained with Hoechst 33342 (for nuclei) and the anti-λ2 (product of the L2 segment) antibody 2 days post inoculation. Images were obtained using the fluorescence microscope with the light cubes for DAPI (for nuclei), GFP (for the λ2 protein), and Texas Red (for KRmem). Merged images are also shown. ( C ) Western blot analysis of infected cells. Each virus was inoculated to BHK/T7-9 cells at an MOI of 100, and the cell lysate was collected 2 days post inoculation. Proteins in the lysate were separated by size, and the σ3 protein (product of the S4 segment), KRmem, and β-actin were probed using specific antibodies on the blotted membrane. Molecular weights are indicated on the left. ( D ) Growth curves of the WT and T3D-L(S2/3′KRmem) viruses in BHK/T7-9 cells. Each virus was inoculated to the cells at an MOI of 0.01, and viral titers in the culture supernatants harvested at the indicated time points were determined. Bars indicate standard deviation, and an asterisk shows the significant difference ( p < 0.05, Student’s t -test, n = 3).

Journal: Pharmaceuticals

Article Title: Cytocidal Effect of Irradiation on Gastric Cancer Cells Infected with a Recombinant Mammalian Orthoreovirus Expressing a Membrane-Targeted KillerRed

doi: 10.3390/ph17010079

Figure Lengend Snippet: Properties of the KRmem-expressing MRV. ( A ) Electrophoretic patterns of genomic dsRNAs extracted from the wild type (WT) or KRmem-expressing virus, T3D-L(S2/3′KRmem). The name of each segment is also indicated. ( B ) Immunofluorescence assay of infected cells. Each virus was inoculated to BHK/T7-9 cells at a multiplicity of infection (MOI) of 100, and cells were fixed and stained with Hoechst 33342 (for nuclei) and the anti-λ2 (product of the L2 segment) antibody 2 days post inoculation. Images were obtained using the fluorescence microscope with the light cubes for DAPI (for nuclei), GFP (for the λ2 protein), and Texas Red (for KRmem). Merged images are also shown. ( C ) Western blot analysis of infected cells. Each virus was inoculated to BHK/T7-9 cells at an MOI of 100, and the cell lysate was collected 2 days post inoculation. Proteins in the lysate were separated by size, and the σ3 protein (product of the S4 segment), KRmem, and β-actin were probed using specific antibodies on the blotted membrane. Molecular weights are indicated on the left. ( D ) Growth curves of the WT and T3D-L(S2/3′KRmem) viruses in BHK/T7-9 cells. Each virus was inoculated to the cells at an MOI of 0.01, and viral titers in the culture supernatants harvested at the indicated time points were determined. Bars indicate standard deviation, and an asterisk shows the significant difference ( p < 0.05, Student’s t -test, n = 3).

Techniques: Expressing, Virus, Immunofluorescence, Infection, Staining, Fluorescence, Microscopy, Western Blot, Membrane, Standard Deviation

Infection of the KRmem-expressing MRV in gastric cancer cell lines. Normal human gastrointestinal epithelial cells (HGEC) and gastric cancer (GC) cell lines (MKN45P and MKN7) were inoculated with T3D-L(S2/3′KRmem) at 2000 TCID 50 /cell. The KRmem expression was observed using the fluorescence microscope with the light cube for Texas Red 7 (normal cells) or 5 (GC cell lines) days post inoculation, and captured fluorescent images are shown in pseudo-color.

Journal: Pharmaceuticals

Article Title: Cytocidal Effect of Irradiation on Gastric Cancer Cells Infected with a Recombinant Mammalian Orthoreovirus Expressing a Membrane-Targeted KillerRed

doi: 10.3390/ph17010079

Figure Lengend Snippet: Infection of the KRmem-expressing MRV in gastric cancer cell lines. Normal human gastrointestinal epithelial cells (HGEC) and gastric cancer (GC) cell lines (MKN45P and MKN7) were inoculated with T3D-L(S2/3′KRmem) at 2000 TCID 50 /cell. The KRmem expression was observed using the fluorescence microscope with the light cube for Texas Red 7 (normal cells) or 5 (GC cell lines) days post inoculation, and captured fluorescent images are shown in pseudo-color.

Techniques: Infection, Expressing, Fluorescence, Microscopy

Photodynamic effect on MKN45P cells infected with the KRmem-expressing MRV. MKN45P cells were inoculated with/without T3D-L(S2/3′KRmem). Two days post inoculation, cells were irradiated with/without an orange laser (589 nm, 172 J/cm 2 ). Afterwards, the cells were incubated in the medium containing the apoptosis/necrosis detection reagent, and ( A ) fluorescence for necrosis and ( B ) luminescence for apoptosis were measured every hour until 48 h after irradiation. Controls indicate cells without both virus infection and light irradiation. Error bands (shaded areas) show the standard error, and p values by one-way ANOVA and Tukey’s multiple comparison test (n = 4) are indicated for 6, 12, 18, and 24 h post irradiation in the right table. The significant differences ( p < 0.05) were highlighted.

Journal: Pharmaceuticals

Article Title: Cytocidal Effect of Irradiation on Gastric Cancer Cells Infected with a Recombinant Mammalian Orthoreovirus Expressing a Membrane-Targeted KillerRed

doi: 10.3390/ph17010079

Figure Lengend Snippet: Photodynamic effect on MKN45P cells infected with the KRmem-expressing MRV. MKN45P cells were inoculated with/without T3D-L(S2/3′KRmem). Two days post inoculation, cells were irradiated with/without an orange laser (589 nm, 172 J/cm 2 ). Afterwards, the cells were incubated in the medium containing the apoptosis/necrosis detection reagent, and ( A ) fluorescence for necrosis and ( B ) luminescence for apoptosis were measured every hour until 48 h after irradiation. Controls indicate cells without both virus infection and light irradiation. Error bands (shaded areas) show the standard error, and p values by one-way ANOVA and Tukey’s multiple comparison test (n = 4) are indicated for 6, 12, 18, and 24 h post irradiation in the right table. The significant differences ( p < 0.05) were highlighted.

Techniques: Infection, Expressing, Irradiation, Incubation, Fluorescence, Virus, Comparison

Schematic diagram of the recombinant viral genome in the genomic plasmid. The MRV S2 segment consists of the viral protein σ2 coding region and 5′ and 3′ untranslated regions (UTRs) at both ends. Its cDNA, together with the ribozyme (Rbz) sequence of the hepatitis D virus, were inserted between the T7 promoter (T7p) and terminator (T7t) sequences in the genome plasmid. The gene cassette consisting of the membrane-targeted and codon-optimized KillerRed gene [KRmem (opt), orange box] and the T2A peptide sequence (black box) were inserted into the 3′ end of the σ2 coding region (nt 19–1275, pale blue box) of the S2 segment using BsiWI and SpeI sites. The cassette was placed upstream of the packaging signal (PS, nt 1234–1331, underlined) located at the 3′ end of the segment. The sequence corresponding to the coding region in PS was not translated because the KRmem gene possessed a stop codon. Several silent mutations were introduced into the duplicated coding region corresponding to PS (mPS, nt 1234–1272, gray blue box) to prevent deletion of the cassette by homologous recombination, and the SpeI site in mPS was simultaneously abolished.

Journal: Pharmaceuticals

Article Title: Cytocidal Effect of Irradiation on Gastric Cancer Cells Infected with a Recombinant Mammalian Orthoreovirus Expressing a Membrane-Targeted KillerRed

doi: 10.3390/ph17010079

Figure Lengend Snippet: Schematic diagram of the recombinant viral genome in the genomic plasmid. The MRV S2 segment consists of the viral protein σ2 coding region and 5′ and 3′ untranslated regions (UTRs) at both ends. Its cDNA, together with the ribozyme (Rbz) sequence of the hepatitis D virus, were inserted between the T7 promoter (T7p) and terminator (T7t) sequences in the genome plasmid. The gene cassette consisting of the membrane-targeted and codon-optimized KillerRed gene [KRmem (opt), orange box] and the T2A peptide sequence (black box) were inserted into the 3′ end of the σ2 coding region (nt 19–1275, pale blue box) of the S2 segment using BsiWI and SpeI sites. The cassette was placed upstream of the packaging signal (PS, nt 1234–1331, underlined) located at the 3′ end of the segment. The sequence corresponding to the coding region in PS was not translated because the KRmem gene possessed a stop codon. Several silent mutations were introduced into the duplicated coding region corresponding to PS (mPS, nt 1234–1272, gray blue box) to prevent deletion of the cassette by homologous recombination, and the SpeI site in mPS was simultaneously abolished.

Techniques: Recombinant, Plasmid Preparation, Sequencing, Virus, Membrane, Homologous Recombination

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1) Product Images from "Snapshot of in-cell protein contact sites reveals new host factors and hijacking of paraspeckles during influenza A virus infection"

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