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rabbit polyclonal anti ifitm3 (Proteintech)

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Proteintech rabbit polyclonal anti ifitm3
Rabbit Polyclonal Anti Ifitm3, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 169 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+ifitm3/IFITM3+Antibody/pmc13016079-3-0-4
Average 95 stars, based on 169 article reviews

rabbit polyclonal anti ifitm3 - by Bioz Stars, 2026-09

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Article Title: Restriction of HIV-1 infectivity by interferon and IFITM3 is counteracted by Nef
Article Snippet: For quantification of HIV-1 infection, TZM-bl cells were fixed with Cytofix/Cytoperm Solution (BD; 554722) and stained with Anti-HIV-1 Core Antigen KC57-FITC (Beckman Coulter; 6604665) for 30 mins at room temperature. .. For cell surface staining of IFITM3, transfected HEK293T were stained with anti-IFITM3 (Proteintech; 66081-1) on ice for 30 mins and then fixed with 2% formaldehyde solution (Invitrogen; FB002) for 10 mins at room temperature. .. Cells were then washed with PBS and stained with secondary antibody goat anti-mouse IgG (H+L) Alexa Fluor 488 (Invitrogen; A11001).

Article Title: Restriction of HIV-1 infectivity by interferon and IFITM3 is counteracted by Nef
Article Snippet: For quantification of HIV-1 infection, TZM-bl cells were fixed with Cytofix/Cytoperm solution (BD, 554722) and stained with Anti-HIV-1 Core Antigen KC57-FITC (Beckman Coulter, 6604665) for 30 min at room temperature. .. For cell surface staining of IFITM3, transfected HEK293T cells were stained with anti-IFITM3 (Proteintech, 66081-1) on ice for 30 min and then fixed with 2% formaldehyde solution (Invitrogen, FB002) for 10 min at room temperature. .. Cells were then washed with PBS and stained with secondary antibody goat anti-mouse IgG (H + L) Alexa Fluor 488 (Invitrogen, A11001).

Transfection:

Article Title: Restriction of HIV-1 infectivity by interferon and IFITM3 is counteracted by Nef
Article Snippet: For quantification of HIV-1 infection, TZM-bl cells were fixed with Cytofix/Cytoperm solution (BD, 554722) and stained with Anti-HIV-1 Core Antigen KC57-FITC (Beckman Coulter, 6604665) for 30 min at room temperature. .. For cell surface staining of IFITM3, transfected HEK293T cells were stained with anti-IFITM3 (Proteintech, 66081-1) on ice for 30 min and then fixed with 2% formaldehyde solution (Invitrogen, FB002) for 10 min at room temperature. .. Cells were then washed with PBS and stained with secondary antibody goat anti-mouse IgG (H + L) Alexa Fluor 488 (Invitrogen, A11001).

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Overexpression of IFITM3 in LPS-stimulated BV2 cells enhances inflammatory responses. ( A ) Venn diagram of the GSE73878 and GSE18740 datasets. ( B ) RT-qPCR analysis demonstrated that IFITM3 was significantly upregulated in the cellular inflammation model. ( C ) The knockdown efficiency of si-IFITM3-1 to -3 was measured by RT-qPCR. ( D ) RT-qPCR analyses and ( E ) western blot were used to detect the effect of IFITM3 overexpression. ( F – H ) Suppression of IFITM3 expression reduced the production of IL-1β, IL-6, and TNF-α in LPS-treated BV2 cells. ( I – K ) The production of IL-1β, IL-6, and TNF-α was enhanced following transfection of IFITM3 into BV2 cells treated with LPS. ( L – N ) The levels of IL-1β, IL-6, and TNF-α were measured using ELISA in LPS-treated BV2 cells transfected with si-IFITM3-2, si-IFITM3-3, IFITM3, or their corresponding negative controls.

Journal: Scientific Reports

Article Title: IFITM3-mediated neuroinflammation in epilepsy regulated by the let-7g-5p/STAT2 axis

doi: 10.1038/s41598-026-44357-z

Figure Lengend Snippet: Overexpression of IFITM3 in LPS-stimulated BV2 cells enhances inflammatory responses. ( A ) Venn diagram of the GSE73878 and GSE18740 datasets. ( B ) RT-qPCR analysis demonstrated that IFITM3 was significantly upregulated in the cellular inflammation model. ( C ) The knockdown efficiency of si-IFITM3-1 to -3 was measured by RT-qPCR. ( D ) RT-qPCR analyses and ( E ) western blot were used to detect the effect of IFITM3 overexpression. ( F – H ) Suppression of IFITM3 expression reduced the production of IL-1β, IL-6, and TNF-α in LPS-treated BV2 cells. ( I – K ) The production of IL-1β, IL-6, and TNF-α was enhanced following transfection of IFITM3 into BV2 cells treated with LPS. ( L – N ) The levels of IL-1β, IL-6, and TNF-α were measured using ELISA in LPS-treated BV2 cells transfected with si-IFITM3-2, si-IFITM3-3, IFITM3, or their corresponding negative controls.

Article Snippet: The primary antibodies targeted STAT2 (rabbit, 1:100; Proteintech) and IFITM3 (mouse, 1:100; Zhongshan Golden Bridge, Beijing, China).

Techniques: Over Expression, Quantitative RT-PCR, Knockdown, Western Blot, Expressing, Transfection, Enzyme-linked Immunosorbent Assay

IFITM3 promotes apoptosis and pyroptosis in LPS-treated BV2 cells. ( A ) The rate of BV2 cells undergoing pyroptosis was quantified by flow cytometry. ( B , C ) The relative expression levels of ASC and IL-18 were determined by RT-qPCR.

Journal: Scientific Reports

Article Title: IFITM3-mediated neuroinflammation in epilepsy regulated by the let-7g-5p/STAT2 axis

doi: 10.1038/s41598-026-44357-z

Figure Lengend Snippet: IFITM3 promotes apoptosis and pyroptosis in LPS-treated BV2 cells. ( A ) The rate of BV2 cells undergoing pyroptosis was quantified by flow cytometry. ( B , C ) The relative expression levels of ASC and IL-18 were determined by RT-qPCR.

Article Snippet: The primary antibodies targeted STAT2 (rabbit, 1:100; Proteintech) and IFITM3 (mouse, 1:100; Zhongshan Golden Bridge, Beijing, China).

Techniques: Flow Cytometry, Expressing, Quantitative RT-PCR

IFITM3 knockdown alleviates seizure severity and neuroinflammatory responses in PTZ-kindled mice. ( A ) Western blot analysis was conducted to assess the expression of IFITM3, verifying the knockdown efficiency of LV-sh-IFITM3 in BV2 cells treated with LPS ( n = 3). ( B ) Severity of seizures was scored according to the Racine scale for the vehicle + LV-sh-NC, PTZ + LV-sh-NC, and PTZ + LV-sh-IFITM3 groups. No seizures were observed in the vehicle + LV-sh-NC group, yielding a score of 0 ( n = 16). ( C ) Representative EEG traces recorded in vivo from each experimental group ( n = 3). ( D – I ) mRNA levels of IFITM3, IL-1β, IL-6, TNF-α, IL-18, and ASC in mouse cortical tissue were determined by RT-qPCR ( n = 16). ( J , K ) Protein levels of IFITM3, cleaved caspase-3, caspase-3, cleaved caspase9, caspase-9, BAX, and BCL2 were evaluated by western blotting in the cortex lysates ( n = 3). Statistical analysis was conducted using two-way ANOVA followed by Bonferroni multiple comparison tests. Data are presented as mean ± standard deviation.

Journal: Scientific Reports

Article Title: IFITM3-mediated neuroinflammation in epilepsy regulated by the let-7g-5p/STAT2 axis

doi: 10.1038/s41598-026-44357-z

Figure Lengend Snippet: IFITM3 knockdown alleviates seizure severity and neuroinflammatory responses in PTZ-kindled mice. ( A ) Western blot analysis was conducted to assess the expression of IFITM3, verifying the knockdown efficiency of LV-sh-IFITM3 in BV2 cells treated with LPS ( n = 3). ( B ) Severity of seizures was scored according to the Racine scale for the vehicle + LV-sh-NC, PTZ + LV-sh-NC, and PTZ + LV-sh-IFITM3 groups. No seizures were observed in the vehicle + LV-sh-NC group, yielding a score of 0 ( n = 16). ( C ) Representative EEG traces recorded in vivo from each experimental group ( n = 3). ( D – I ) mRNA levels of IFITM3, IL-1β, IL-6, TNF-α, IL-18, and ASC in mouse cortical tissue were determined by RT-qPCR ( n = 16). ( J , K ) Protein levels of IFITM3, cleaved caspase-3, caspase-3, cleaved caspase9, caspase-9, BAX, and BCL2 were evaluated by western blotting in the cortex lysates ( n = 3). Statistical analysis was conducted using two-way ANOVA followed by Bonferroni multiple comparison tests. Data are presented as mean ± standard deviation.

Article Snippet: The primary antibodies targeted STAT2 (rabbit, 1:100; Proteintech) and IFITM3 (mouse, 1:100; Zhongshan Golden Bridge, Beijing, China).

Techniques: Knockdown, Western Blot, Expressing, In Vivo, Quantitative RT-PCR, Comparison, Standard Deviation

STAT2 as a potential transcription factor for IFITM3. ( A ) The expression levels of transcription factors IRF9, STAT2, MAFF, TFAP2C, and PITX2 in BV2 cells were measured, with Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) serving as the internal control. The overexpression efficiency of ( B ) IRF9 or ( C ) STAT2 plasmids was measured. ( D ) The inhibition efficiency of four si-IRF9 constructs was assessed in BV2 cells using RT-qPCR. ( E ) The inhibition efficiency of four si-IFITM3 constructs was similarly evaluated in BV2 cells. IFITM3 expression was evaluated by RT-qPCR in BV2 cells transfected with ( F ) IRF9 or ( G ) STAT2. RT-qPCR was performed to quantify IFITM3 expression in BV2 cells transfected with ( H ) si-IRF9-1 or ( I ) si-STAT2-3. ( J ) HEK293T cells were co-transfected with the IFITM3 promoter and negative control, IRF9, or STAT2 plasmids. After 48 h, luciferase activity and corresponding protein expression were detected. ( K ) BV2 cells were co-transfected with STAT2 or negative control together with either the IFITM3 promoter or IFITM3-promoter-mut. The relative luciferase activity was measured. ( L ) IFITM3 protein levels were examined by western blot in BV2 cells transfected with si-NC, si-STAT2-3, si-STAT2-4, oe-NC or STAT2. ( M ) Representative immunofluorescence images (magnification ×400) demonstrate the expression of IFITM3. Blue: nuclear staining (DAPI); red: IFITM3 staining. Scale bar: 100 μm. STAT2 expression in the cortex ( N ) and hippocampus ( O ) of epileptic mice was assessed by RT-qPCR ( n = 16).

Journal: Scientific Reports

Article Title: IFITM3-mediated neuroinflammation in epilepsy regulated by the let-7g-5p/STAT2 axis

doi: 10.1038/s41598-026-44357-z

Figure Lengend Snippet: STAT2 as a potential transcription factor for IFITM3. ( A ) The expression levels of transcription factors IRF9, STAT2, MAFF, TFAP2C, and PITX2 in BV2 cells were measured, with Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) serving as the internal control. The overexpression efficiency of ( B ) IRF9 or ( C ) STAT2 plasmids was measured. ( D ) The inhibition efficiency of four si-IRF9 constructs was assessed in BV2 cells using RT-qPCR. ( E ) The inhibition efficiency of four si-IFITM3 constructs was similarly evaluated in BV2 cells. IFITM3 expression was evaluated by RT-qPCR in BV2 cells transfected with ( F ) IRF9 or ( G ) STAT2. RT-qPCR was performed to quantify IFITM3 expression in BV2 cells transfected with ( H ) si-IRF9-1 or ( I ) si-STAT2-3. ( J ) HEK293T cells were co-transfected with the IFITM3 promoter and negative control, IRF9, or STAT2 plasmids. After 48 h, luciferase activity and corresponding protein expression were detected. ( K ) BV2 cells were co-transfected with STAT2 or negative control together with either the IFITM3 promoter or IFITM3-promoter-mut. The relative luciferase activity was measured. ( L ) IFITM3 protein levels were examined by western blot in BV2 cells transfected with si-NC, si-STAT2-3, si-STAT2-4, oe-NC or STAT2. ( M ) Representative immunofluorescence images (magnification ×400) demonstrate the expression of IFITM3. Blue: nuclear staining (DAPI); red: IFITM3 staining. Scale bar: 100 μm. STAT2 expression in the cortex ( N ) and hippocampus ( O ) of epileptic mice was assessed by RT-qPCR ( n = 16).

Article Snippet: The primary antibodies targeted STAT2 (rabbit, 1:100; Proteintech) and IFITM3 (mouse, 1:100; Zhongshan Golden Bridge, Beijing, China).

Techniques: Expressing, Control, Over Expression, Inhibition, Construct, Quantitative RT-PCR, Transfection, Negative Control, Luciferase, Activity Assay, Western Blot, Immunofluorescence, Staining

STAT2 promotes inflammation, apoptosis, and pyroptosis through modulation of IFITM3. ( A – C ) Levels of IL-1β, IL-6, and TNF-α were quantified in BV2 cells transfected with STAT2, si-IFITM3-3, or the corresponding negative controls. The rescue experiments involved co-transfection of STAT2 with si-IFITM3-3. ( D – F ) The expression levels of IL-1β, IL-6, and TNF-α in BV2 cells transfected with si-STAT2-3, IFITM3, or the respective negative controls. The rescue experiments involved co-transfection of si-STAT2-3 with IFITM3. ( G ) The apoptosis rate of BV2 cells transfected with si-STAT2-3, IFITM3, or their negative controls. ( H ) Flow cytometry was performed to assess apoptosis rate in each treatment group. The expression levels of ( I , K ) ASC and ( J , L ) IL-18 in BV2 cells treated with different plasmids were detected by RT-qPCR analysis.

Journal: Scientific Reports

Article Title: IFITM3-mediated neuroinflammation in epilepsy regulated by the let-7g-5p/STAT2 axis

doi: 10.1038/s41598-026-44357-z

Figure Lengend Snippet: STAT2 promotes inflammation, apoptosis, and pyroptosis through modulation of IFITM3. ( A – C ) Levels of IL-1β, IL-6, and TNF-α were quantified in BV2 cells transfected with STAT2, si-IFITM3-3, or the corresponding negative controls. The rescue experiments involved co-transfection of STAT2 with si-IFITM3-3. ( D – F ) The expression levels of IL-1β, IL-6, and TNF-α in BV2 cells transfected with si-STAT2-3, IFITM3, or the respective negative controls. The rescue experiments involved co-transfection of si-STAT2-3 with IFITM3. ( G ) The apoptosis rate of BV2 cells transfected with si-STAT2-3, IFITM3, or their negative controls. ( H ) Flow cytometry was performed to assess apoptosis rate in each treatment group. The expression levels of ( I , K ) ASC and ( J , L ) IL-18 in BV2 cells treated with different plasmids were detected by RT-qPCR analysis.

Article Snippet: The primary antibodies targeted STAT2 (rabbit, 1:100; Proteintech) and IFITM3 (mouse, 1:100; Zhongshan Golden Bridge, Beijing, China).

Techniques: Transfection, Cotransfection, Expressing, Flow Cytometry, Quantitative RT-PCR

(A) HEK293 cells transfected with Flag-ZMPSTE24 or Flag-ZMPSTE24 E336A and myc-IFITM3 were subjected to co-IP with anti-Flag agarose beads. Immune complexes were resolved by non-reducing (left) or reducing (right) SDS-PAGE prior to Western blotting with anti-Flag and anti-myc antibodies. A higher molecular weight species (∼65 kDa) containing both the myc and Flag signals is detected exclusively under non-reducing conditions. (B) The disulfide-linked species containing ZMPSTE24 E336A and IFITM3 is disrupted by NEM in the lysis buffer. Cells transfected with Flag-ZMPSTE24 E336A were induced with interferon β for 18 hrs prior to lysis with 1% Triton X-100 buffer without (-) or with (+) 0.1mM NEM. Proteins were immunoprecipitated with anti-Flag agarose beads, resolved by non-reducing SDS-PAGE and analyzed by Western blotting with anti-Flag and anti-IFITM3 antibodies. * denotes a non-specific background band. (C) HEK293 cells were transfected with vector, Flag-ZMPSTE24 or Flag-ZMPSTE24 E336A with the indicated myc-tagged IFITM3 cysteine variants and subjected to co-IP followed by non-reducing SDS-PAGE and Western blotting. The IFITM3-C71A mutant fails to bind ZMPSTE24 altogether, and the ZMPSTE24 E336A -IFITM3 intermolecular disulfide complex is absent for the IFITM3-C105A mutant.

Journal: bioRxiv

Article Title: The zinc metalloprotease ZMPSTE24 binds a distinct topological isoform of the tail-anchored protein IFITM3

doi: 10.64898/2026.02.27.708584

Figure Lengend Snippet: (A) HEK293 cells transfected with Flag-ZMPSTE24 or Flag-ZMPSTE24 E336A and myc-IFITM3 were subjected to co-IP with anti-Flag agarose beads. Immune complexes were resolved by non-reducing (left) or reducing (right) SDS-PAGE prior to Western blotting with anti-Flag and anti-myc antibodies. A higher molecular weight species (∼65 kDa) containing both the myc and Flag signals is detected exclusively under non-reducing conditions. (B) The disulfide-linked species containing ZMPSTE24 E336A and IFITM3 is disrupted by NEM in the lysis buffer. Cells transfected with Flag-ZMPSTE24 E336A were induced with interferon β for 18 hrs prior to lysis with 1% Triton X-100 buffer without (-) or with (+) 0.1mM NEM. Proteins were immunoprecipitated with anti-Flag agarose beads, resolved by non-reducing SDS-PAGE and analyzed by Western blotting with anti-Flag and anti-IFITM3 antibodies. * denotes a non-specific background band. (C) HEK293 cells were transfected with vector, Flag-ZMPSTE24 or Flag-ZMPSTE24 E336A with the indicated myc-tagged IFITM3 cysteine variants and subjected to co-IP followed by non-reducing SDS-PAGE and Western blotting. The IFITM3-C71A mutant fails to bind ZMPSTE24 altogether, and the ZMPSTE24 E336A -IFITM3 intermolecular disulfide complex is absent for the IFITM3-C105A mutant.

Article Snippet: Anti-IFITM3 (Proteintech, 11714-1-AP) was used at 1:10,000.

Techniques: Transfection, Co-Immunoprecipitation Assay, SDS Page, Western Blot, Molecular Weight, Lysis, Immunoprecipitation, Plasmid Preparation, Mutagenesis

Cells expressing Flag-ZMPSTE24 E336A were induced with interferon β for 18 hrs. Cells were lysed in buffer containing 1% Triton X-100, 1% dodecyl maltoside (DDM) or 1% digitonin prior to immunoprecipitation with anti-Flag agarose beads. Proteins were resolved by non-reducing SDS-PAGE and analyzed by Western blotting with anti-Flag and anti-IFITM3 antibodies. Positions of IFITM3, Flag-ZMPSTE24 E336A and the intermolecular disulfide-linked complex are shown.

Journal: bioRxiv

Article Title: The zinc metalloprotease ZMPSTE24 binds a distinct topological isoform of the tail-anchored protein IFITM3

doi: 10.64898/2026.02.27.708584

Figure Lengend Snippet: Cells expressing Flag-ZMPSTE24 E336A were induced with interferon β for 18 hrs. Cells were lysed in buffer containing 1% Triton X-100, 1% dodecyl maltoside (DDM) or 1% digitonin prior to immunoprecipitation with anti-Flag agarose beads. Proteins were resolved by non-reducing SDS-PAGE and analyzed by Western blotting with anti-Flag and anti-IFITM3 antibodies. Positions of IFITM3, Flag-ZMPSTE24 E336A and the intermolecular disulfide-linked complex are shown.

Article Snippet: Anti-IFITM3 (Proteintech, 11714-1-AP) was used at 1:10,000.

Techniques: Expressing, Immunoprecipitation, SDS Page, Western Blot

Protein expression of ISG in rNLS8 brains. A . Expression of IFIT3 and ISG15 protein at different time points after induction of disease in rNLS8 mice (source https://shiny.rcc.uq.edu.au/TDP-map . B . Representative examples of immunohistochemical (IHC) staining in the region of the hippocampus of control and rNLS8 mice with the antibodies against the antigens indicated. Wild type (control) mouse on top row; rNLS8 mouse bottom row. Left column: brown indicates positive staining for ISG15; blue, hematoxylin counterstain. Original magnification 20x; bar = 100 microns. Right column: brown indicates positive staining for IFITM3, blue, hematoxylin counterstain. Original magnification 20x, bar = 100 microns. Inset bars = 50 microns. “n” = neurons of the hippocampus. C . Semi-quantitative scoring of IFITM3 and ISG15 in the brains of control and rNLS mice (n=4 per group, scores for individual mice are represented by circles [control mice] and boxes [rNLS8] mice on the graph). Y-axis is the semi-quantitative score from 0–4 (see Methods). P -values were calculated using the unpaired nonparametric Mann-Whitney t-test (GraphPad Prism 10 Software) (* indicates p < 0.05) D . Three color immunofluorescence of formalin-fixed paraffin-embedded tissues from control and rNLS8 mouse in the region of the hippocampus was performed as described in Methods. Bar = 100 microns. Red indicates NeuN expression (neurons); green indicates GFAP expression (astrocytes); yellow indicates ISG15 expression; blue indicates DAPI expression (nuclei). White arrows mark regions of ISG15 expression associated with GFAP expression. Inset also shows co-localizing astrocyte (green) and ISG15 (yellow) expression. E . Upper panel. Quantitative analysis of ISG15 expression in the region of the hippocampus in control and rNLS8 mice ( n =4 per group), Y-axis is the percent positive ISG15 expression (see Methods). P -values were calculated using the unpaired nonparametric Mann-Whitney t-test (GraphPad Prism 10 Software) (* indicates p < 0.05). Lower panel. Quantitative analysis of the percentage of ISG15 within GFAP in the region of the hippocampus in control and rNLS8 mice

Journal: Journal of Neuroinflammation

Article Title: Neuronal TDP-43 pathology drives astrocytic interferon response in a mouse model of ALS

doi: 10.1186/s12974-025-03658-2

Figure Lengend Snippet: Protein expression of ISG in rNLS8 brains. A . Expression of IFIT3 and ISG15 protein at different time points after induction of disease in rNLS8 mice (source https://shiny.rcc.uq.edu.au/TDP-map . B . Representative examples of immunohistochemical (IHC) staining in the region of the hippocampus of control and rNLS8 mice with the antibodies against the antigens indicated. Wild type (control) mouse on top row; rNLS8 mouse bottom row. Left column: brown indicates positive staining for ISG15; blue, hematoxylin counterstain. Original magnification 20x; bar = 100 microns. Right column: brown indicates positive staining for IFITM3, blue, hematoxylin counterstain. Original magnification 20x, bar = 100 microns. Inset bars = 50 microns. “n” = neurons of the hippocampus. C . Semi-quantitative scoring of IFITM3 and ISG15 in the brains of control and rNLS mice (n=4 per group, scores for individual mice are represented by circles [control mice] and boxes [rNLS8] mice on the graph). Y-axis is the semi-quantitative score from 0–4 (see Methods). P -values were calculated using the unpaired nonparametric Mann-Whitney t-test (GraphPad Prism 10 Software) (* indicates p < 0.05) D . Three color immunofluorescence of formalin-fixed paraffin-embedded tissues from control and rNLS8 mouse in the region of the hippocampus was performed as described in Methods. Bar = 100 microns. Red indicates NeuN expression (neurons); green indicates GFAP expression (astrocytes); yellow indicates ISG15 expression; blue indicates DAPI expression (nuclei). White arrows mark regions of ISG15 expression associated with GFAP expression. Inset also shows co-localizing astrocyte (green) and ISG15 (yellow) expression. E . Upper panel. Quantitative analysis of ISG15 expression in the region of the hippocampus in control and rNLS8 mice ( n =4 per group), Y-axis is the percent positive ISG15 expression (see Methods). P -values were calculated using the unpaired nonparametric Mann-Whitney t-test (GraphPad Prism 10 Software) (* indicates p < 0.05). Lower panel. Quantitative analysis of the percentage of ISG15 within GFAP in the region of the hippocampus in control and rNLS8 mice

Article Snippet: The following primary polyclonal antibodies were used: rabbit anti-mouse IFITM3 antibody, clone RB13975 (Antibodies online, Limerick, PA, catalog # ABIN2845007) at 1:1,000; rabbit anti-mouse ISG15 antibody (Proteintech, Rosemont, IL, catalog #15981–1-AP) at 1:300.

Techniques: Expressing, Immunohistochemical staining, Immunohistochemistry, Control, Staining, MANN-WHITNEY, Software, Immunofluorescence, Formalin-fixed Paraffin-Embedded

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rabbit polyclonal anti ifitm3 (Proteintech)

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