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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
https://www.bioz.com/result/slc7a5 mouse monoclonal/product/Proteintech
Average 95 stars, based on 1 article reviews

slc7a5 mouse monoclonal - by Bioz Stars, 2025-05

95/100 stars

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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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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

SLC7A5 expression in fibroblast-like synoviocytes of RA patients. a Hematoxylin and eosin (H&E) staining of the synovial tissue from RA and OA patients. Black arrows represent the lining cells of synovial tissues, the blue arrows represent the inflamed cells in synovial tissues. b The mRNA expression of SLC7A5 in synovial tissue from OA and RA patients, detected by RT-qPCR (RA n = 15, OA n = 14). Correlation analysis of SLC7A5 mRNA expression in FLS from RA patients ( n = 15) with RF ( c ) and CRP ( d ). e The protein expression of SLC7A5 in synovial tissues from OA and RA patients detected by Western blotting. The density of SLC7A5 immune-reactive bands was analyzed by using ACTB expression as a loading control (RA n = 22, OA n = 22). f Representative immunofluorescence staining for SLC7A5 (green) and vimentin (red) in synovial tissue from OA and RA patients (RA n = 3, OA n = 3). The slide used for IF stain was consecutively followed slide stained with H&E. The picture shown in f was the enlarging arrow area pointed out in a . The yellow boxes were amplified in g , yellow arrow pointed out the representative staining cells (* p < 0.05)

Journal: Arthritis Research & Therapy

Article Title: Intervening upregulated SLC7A5 could mitigate inflammatory mediator by mTOR-P70S6K signal in rheumatoid arthritis synoviocytes

doi: 10.1186/s13075-020-02296-8

Figure Lengend Snippet: SLC7A5 expression in fibroblast-like synoviocytes of RA patients. a Hematoxylin and eosin (H&E) staining of the synovial tissue from RA and OA patients. Black arrows represent the lining cells of synovial tissues, the blue arrows represent the inflamed cells in synovial tissues. b The mRNA expression of SLC7A5 in synovial tissue from OA and RA patients, detected by RT-qPCR (RA n = 15, OA n = 14). Correlation analysis of SLC7A5 mRNA expression in FLS from RA patients ( n = 15) with RF ( c ) and CRP ( d ). e The protein expression of SLC7A5 in synovial tissues from OA and RA patients detected by Western blotting. The density of SLC7A5 immune-reactive bands was analyzed by using ACTB expression as a loading control (RA n = 22, OA n = 22). f Representative immunofluorescence staining for SLC7A5 (green) and vimentin (red) in synovial tissue from OA and RA patients (RA n = 3, OA n = 3). The slide used for IF stain was consecutively followed slide stained with H&E. The picture shown in f was the enlarging arrow area pointed out in a . The yellow boxes were amplified in g , yellow arrow pointed out the representative staining cells (* p < 0.05)

Article Snippet: For immunofluorescence staining, 6-μm-thick tissue sections were incubated overnight at 4 °C with the following primary antibodies diluted in PBS: mouse monoclonal antibody against SLC7A5 (1:100, Santa Cruz, sc-374232) and rabbit polyclonal antibody to vimentin (1:100, Bioss, bs-23064R).

Techniques: Expressing, Staining, Quantitative RT-PCR, Western Blot, Immunofluorescence, Amplification

Mechanism of SLC7A5 upregulation in fibroblast-like synoviocytes (FLS) under IL-1β treatment. a The protein expression of SLC7A5 in FLS from RA patients treated with different cytokines (IL-1β 20 ng/mL, TNF-α 10 ng/mL, IFN-γ 20 ng/mL, IL-6 20 ng/mL, and IL-17A 10 ng/mL) for 24 h, detected by Western blotting. The density of SLC7A5 immune-reactive bands was analyzed by using ACTB expression as a loading control ( n = 3). b The representative active signaling pathways in FLS from RA patients, detected by Western blotting. The cells were treated with 20 ng/mL IL-1β and collected at different time points for protein isolation. c The mRNA levels of SLC7A5 in FLS from RA patients incubated with different inhibitors and stimulated with IL-1β. The cells were firstly treated with NF-κB inhibitor Bay 11-7085 (10 μM) or JNK inhibitor SP600125 (10 μM) for 4 h and then treated with 20 ng/mL IL-1β for 24 h. The mRNA expression was detected by RT-qPCR ( n = 6). d The protein expression of SLC7A5 in FLS from RA patients incubated with different inhibitors and stimulated with IL-1β. The cells were firstly treated with NF-κB inhibitor Bay 11-7085 (10 μM) or JNK inhibitor SP600125 (10 μM) for 4 h and then treated with 20 ng/mL IL-1β for 24 h. The protein expression was detected by Western blotting. The SLC7A5 immune-reactive band density was analyzed by using ACTB expression as a loading control ( n = 3). e The protein expression of SLC7A5 in FLS from RA patients incubated with p38 inhibitor and stimulated with IL-1β. The cells were firstly treated with p38 inhibitor SB203580 (10 μM) for 4 h and then treated with 20 ng/mL IL-1β for 24 h. The protein expression was detected by Western blotting. SLC7A5 immune-reactive bands density was analyzed by using ACTB expression as a loading control ( n = 3) (* p < 0.05)

Journal: Arthritis Research & Therapy

Article Title: Intervening upregulated SLC7A5 could mitigate inflammatory mediator by mTOR-P70S6K signal in rheumatoid arthritis synoviocytes

doi: 10.1186/s13075-020-02296-8

Figure Lengend Snippet: Mechanism of SLC7A5 upregulation in fibroblast-like synoviocytes (FLS) under IL-1β treatment. a The protein expression of SLC7A5 in FLS from RA patients treated with different cytokines (IL-1β 20 ng/mL, TNF-α 10 ng/mL, IFN-γ 20 ng/mL, IL-6 20 ng/mL, and IL-17A 10 ng/mL) for 24 h, detected by Western blotting. The density of SLC7A5 immune-reactive bands was analyzed by using ACTB expression as a loading control ( n = 3). b The representative active signaling pathways in FLS from RA patients, detected by Western blotting. The cells were treated with 20 ng/mL IL-1β and collected at different time points for protein isolation. c The mRNA levels of SLC7A5 in FLS from RA patients incubated with different inhibitors and stimulated with IL-1β. The cells were firstly treated with NF-κB inhibitor Bay 11-7085 (10 μM) or JNK inhibitor SP600125 (10 μM) for 4 h and then treated with 20 ng/mL IL-1β for 24 h. The mRNA expression was detected by RT-qPCR ( n = 6). d The protein expression of SLC7A5 in FLS from RA patients incubated with different inhibitors and stimulated with IL-1β. The cells were firstly treated with NF-κB inhibitor Bay 11-7085 (10 μM) or JNK inhibitor SP600125 (10 μM) for 4 h and then treated with 20 ng/mL IL-1β for 24 h. The protein expression was detected by Western blotting. The SLC7A5 immune-reactive band density was analyzed by using ACTB expression as a loading control ( n = 3). e The protein expression of SLC7A5 in FLS from RA patients incubated with p38 inhibitor and stimulated with IL-1β. The cells were firstly treated with p38 inhibitor SB203580 (10 μM) for 4 h and then treated with 20 ng/mL IL-1β for 24 h. The protein expression was detected by Western blotting. SLC7A5 immune-reactive bands density was analyzed by using ACTB expression as a loading control ( n = 3) (* p < 0.05)

Techniques: Expressing, Western Blot, Isolation, Incubation, Quantitative RT-PCR

Impact of SLC7A5 intervention either by antibody blocking or siRNA knockdown on the expression levels of MMP3 and MMP13 in FLS from RA patients. a The mRNA expression of MMP13 and MMP3 in RA FLS, incubated with SLC7A5 monoclonal antibody or isotype IgG and stimulated with or without IL-1β. The cells were incubated with SLC7A5 monoclonal antibody or isotype IgG for 4 h and then treated with or without IL-1β (20 ng/mL) for 8 h. The mRNA levels were measured by RT-qPCR ( n = 6). b The protein expression of MMP13 and MMP3 in RA FLS, incubated with SLC7A5 monoclonal antibody or isotype IgG and stimulated with or without IL-1β. The cells were incubated with SLC7A5 monoclonal antibody or isotype IgG 4 h and then treated with or without IL-1β (20 ng/mL) for 24 h. The protein levels were detected by Western blotting. The density of MMP13 and MMP3 immune-reactive bands was analyzed by using ACTB expression as a loading control ( n = 3). c , d Optimization of the SLC7A5 RNAi efficiency in FLS from RA patients. The cells were transfected with siRNA (NC, siSLC7A5-1 or 2) for 24 h, and the protein and mRNA expression levels were detected by Western blotting ( c ) and RT-qPCR ( d ), respectively. e – g The expression of SLC7A5 , MMP13 , and MMP3 in FLS from RA patients transfected with siRNA (NC or siSLC7A5-2) and treated with or without IL-1β, detected at the mRNA level by RT-qPCR. The cells were first transfected with siRNA (NC or siSLC7A5-2) for 24 h and then treated with or without IL-1β (20 ng/mL) for 8 h without changing the culture medium. h The protein expression of SLC7A5, MMP13, and MMP3 in FLS from RA patients transfected with siRNA (NC or siSLC7A5-2) and treated with or without IL-1β. The cells were first transfected with siRNA (NC or siSLC7A5-2) for 24 h and then treated with or without IL-1β (20 ng/mL) for 24 h further, without changing the culture medium. The density of MMP13 and MMP3 immune-reactive bands was analyzed by using ACTB expression as a loading control ( n = 3) (* p < 0.05)

Journal: Arthritis Research & Therapy

Article Title: Intervening upregulated SLC7A5 could mitigate inflammatory mediator by mTOR-P70S6K signal in rheumatoid arthritis synoviocytes

doi: 10.1186/s13075-020-02296-8

Figure Lengend Snippet: Impact of SLC7A5 intervention either by antibody blocking or siRNA knockdown on the expression levels of MMP3 and MMP13 in FLS from RA patients. a The mRNA expression of MMP13 and MMP3 in RA FLS, incubated with SLC7A5 monoclonal antibody or isotype IgG and stimulated with or without IL-1β. The cells were incubated with SLC7A5 monoclonal antibody or isotype IgG for 4 h and then treated with or without IL-1β (20 ng/mL) for 8 h. The mRNA levels were measured by RT-qPCR ( n = 6). b The protein expression of MMP13 and MMP3 in RA FLS, incubated with SLC7A5 monoclonal antibody or isotype IgG and stimulated with or without IL-1β. The cells were incubated with SLC7A5 monoclonal antibody or isotype IgG 4 h and then treated with or without IL-1β (20 ng/mL) for 24 h. The protein levels were detected by Western blotting. The density of MMP13 and MMP3 immune-reactive bands was analyzed by using ACTB expression as a loading control ( n = 3). c , d Optimization of the SLC7A5 RNAi efficiency in FLS from RA patients. The cells were transfected with siRNA (NC, siSLC7A5-1 or 2) for 24 h, and the protein and mRNA expression levels were detected by Western blotting ( c ) and RT-qPCR ( d ), respectively. e – g The expression of SLC7A5 , MMP13 , and MMP3 in FLS from RA patients transfected with siRNA (NC or siSLC7A5-2) and treated with or without IL-1β, detected at the mRNA level by RT-qPCR. The cells were first transfected with siRNA (NC or siSLC7A5-2) for 24 h and then treated with or without IL-1β (20 ng/mL) for 8 h without changing the culture medium. h The protein expression of SLC7A5, MMP13, and MMP3 in FLS from RA patients transfected with siRNA (NC or siSLC7A5-2) and treated with or without IL-1β. The cells were first transfected with siRNA (NC or siSLC7A5-2) for 24 h and then treated with or without IL-1β (20 ng/mL) for 24 h further, without changing the culture medium. The density of MMP13 and MMP3 immune-reactive bands was analyzed by using ACTB expression as a loading control ( n = 3) (* p < 0.05)

Techniques: Blocking Assay, Expressing, Incubation, Quantitative RT-PCR, Western Blot, Transfection

SLC7A5 impact on the production of cytokines and chemokines in RA FLS. a Images of cytokine array membranes incubated with supernatants from RA FLS, transfected with NC or SLC7A5 siRNA (si-2). The cells were transfected with either negative control or SLC7A5 siRNA (si-2) for 48 h. All the cytokine and chemokine fold change is shown in the heat map. b Semi-quantitative data showing altered cytokine expression (fold change beyond ± 1.5) in RA FLS supernatants 48 h post-siRNA transfection. c KEGG pathway analysis of the differentially expressed cytokines and chemokines in RA FLS

Journal: Arthritis Research & Therapy

Article Title: Intervening upregulated SLC7A5 could mitigate inflammatory mediator by mTOR-P70S6K signal in rheumatoid arthritis synoviocytes

doi: 10.1186/s13075-020-02296-8

Figure Lengend Snippet: SLC7A5 impact on the production of cytokines and chemokines in RA FLS. a Images of cytokine array membranes incubated with supernatants from RA FLS, transfected with NC or SLC7A5 siRNA (si-2). The cells were transfected with either negative control or SLC7A5 siRNA (si-2) for 48 h. All the cytokine and chemokine fold change is shown in the heat map. b Semi-quantitative data showing altered cytokine expression (fold change beyond ± 1.5) in RA FLS supernatants 48 h post-siRNA transfection. c KEGG pathway analysis of the differentially expressed cytokines and chemokines in RA FLS

Techniques: Incubation, Transfection, Negative Control, Expressing

Activation of mTOR-P70S6K signaling and downstream upregulation of MMP3 and MMP13 expression by SLC7A5 overexpressed in RA FLS. a The protein expression of p-mTOR ( n = 4), mTOR, and P70S6K ( n = 3) in synovial tissue from OA and RA patients detected by Western blotting. b The protein synthesis pathway activation in FLS. The FLS were treated with 20 ng/mL IL-1β for 4 h and collected for protein isolation, detected by Western blotting. The density of SLC7A5 immune-reactive bands was analyzed by using ACTB expression as a loading control. The phosphorylation protein ratio fold change of mTOR and P70S6K was analyzed by using total protein expression of their own as a control, while the phosphorylation protein ratio fold change of 4EBP1 was analyzed by using ACTB expression as a loading control ( n = 3). c The impact of SLC7A5 siRNA on the protein synthesis pathway (mTOR-P70S6K-4EBP1) activation in FLS, detected by Western blotting. The cells were transfected with siNC or siSLC7A5 (si-2) for 24 h and then stimulated with 20 ng/mL IL-1β for another 4 h. The fold change in phosphorylated/non-phosphorylated protein ratios of mTOR and P70S6K was analyzed by using total protein expression of their own as a control, while that of 4EBP1 was analyzed by using ACTB expression as a loading control ( n = 3). d The inhibition of MMP3 and MMP13 expression by rapamycin (mTORC1 inhibitor) in RA FLS under IL-1β treatment. The cells were incubated with rapamycin (100 nM) for 8 h and then stimulated with 20 ng/mL IL-1β for another 24 h. The protein levels were detected by Western blotting. The density of MMP3 and MMP13 immune-reactive bands was analyzed by using ACTB expression as a loading control ( n = 3) (* p < 0.05)

Journal: Arthritis Research & Therapy

Article Title: Intervening upregulated SLC7A5 could mitigate inflammatory mediator by mTOR-P70S6K signal in rheumatoid arthritis synoviocytes

doi: 10.1186/s13075-020-02296-8

Figure Lengend Snippet: Activation of mTOR-P70S6K signaling and downstream upregulation of MMP3 and MMP13 expression by SLC7A5 overexpressed in RA FLS. a The protein expression of p-mTOR ( n = 4), mTOR, and P70S6K ( n = 3) in synovial tissue from OA and RA patients detected by Western blotting. b The protein synthesis pathway activation in FLS. The FLS were treated with 20 ng/mL IL-1β for 4 h and collected for protein isolation, detected by Western blotting. The density of SLC7A5 immune-reactive bands was analyzed by using ACTB expression as a loading control. The phosphorylation protein ratio fold change of mTOR and P70S6K was analyzed by using total protein expression of their own as a control, while the phosphorylation protein ratio fold change of 4EBP1 was analyzed by using ACTB expression as a loading control ( n = 3). c The impact of SLC7A5 siRNA on the protein synthesis pathway (mTOR-P70S6K-4EBP1) activation in FLS, detected by Western blotting. The cells were transfected with siNC or siSLC7A5 (si-2) for 24 h and then stimulated with 20 ng/mL IL-1β for another 4 h. The fold change in phosphorylated/non-phosphorylated protein ratios of mTOR and P70S6K was analyzed by using total protein expression of their own as a control, while that of 4EBP1 was analyzed by using ACTB expression as a loading control ( n = 3). d The inhibition of MMP3 and MMP13 expression by rapamycin (mTORC1 inhibitor) in RA FLS under IL-1β treatment. The cells were incubated with rapamycin (100 nM) for 8 h and then stimulated with 20 ng/mL IL-1β for another 24 h. The protein levels were detected by Western blotting. The density of MMP3 and MMP13 immune-reactive bands was analyzed by using ACTB expression as a loading control ( n = 3) (* p < 0.05)

Techniques: Activation Assay, Expressing, Western Blot, Isolation, Transfection, Inhibition, Incubation

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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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