Review

anti mouse fh antibody (Hycult Biotech)

Name: anti mouse fh antibody
Brand: Hycult Biotech
Rating: 94 (4 reviews)

Hycult Biotech is a verified supplier

Hycult Biotech manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Hycult Biotech anti mouse fh antibody
Anti Mouse Fh Antibody, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti mouse fh antibody/product/Hycult Biotech
Average 94 stars, based on 1 article reviews

anti mouse fh antibody - by Bioz Stars, 2025-03

94/100 stars

Images

Image Search Results

( a ) ChPs were stained for C1q (red) and C4 (green). Bar 100 µm. ( b ) C5 siRNA treatment blocks C5 protein deposition in ApoE-/- ChPs; ( c ) ChPs were stained for C3. Ig represents lipid; ( d ) Serum C3 and C5. Serum C3 and C5 protein levels were measured by ELISA. ApoE-/-(n = 6 mice), HFD ApoE4 (n=5). ( e ) High resolution confocal microscopy shows colocalization of ApoE4 (ApoE, red) and Ig (green, represents lipid) in HFD ApoE4-KI ChPs. ApoE-/- ChPs serve as negative controls for ApoE staining; ( f) Complement regulators are expressed in ChPs. WT (n = 5 mice); ApoE-/-(n=4); ND ApoE3 (n=6); HFD ApoE3 (n=6); ND ApoE4 (n=6); HFD ApoE4 (n=6). ( g ) ChP Factor H expressed between WT and ApoE-/- mice. WT (n=5); ApoE-/-(n=4); (h) ChP factor H protein in ChPs. White arrows indicate lipid positive areas. Data in a,b,c,e,h are representative images from at least 3 biologically independent mouse samples. Data in d,f,g represent means ± SEM; Two-tailed Student's t-test was applied to d,g; one-way ANOVA with Tukey posttest was applied to f; Gene names in .

Journal: Nature medicine

Article Title: ApoE attenuates unresolvable inflammation by complex formation with activated C1q

doi: 10.1038/s41591-018-0336-8

Figure Lengend Snippet: ( a ) ChPs were stained for C1q (red) and C4 (green). Bar 100 µm. ( b ) C5 siRNA treatment blocks C5 protein deposition in ApoE-/- ChPs; ( c ) ChPs were stained for C3. Ig represents lipid; ( d ) Serum C3 and C5. Serum C3 and C5 protein levels were measured by ELISA. ApoE-/-(n = 6 mice), HFD ApoE4 (n=5). ( e ) High resolution confocal microscopy shows colocalization of ApoE4 (ApoE, red) and Ig (green, represents lipid) in HFD ApoE4-KI ChPs. ApoE-/- ChPs serve as negative controls for ApoE staining; ( f) Complement regulators are expressed in ChPs. WT (n = 5 mice); ApoE-/-(n=4); ND ApoE3 (n=6); HFD ApoE3 (n=6); ND ApoE4 (n=6); HFD ApoE4 (n=6). ( g ) ChP Factor H expressed between WT and ApoE-/- mice. WT (n=5); ApoE-/-(n=4); (h) ChP factor H protein in ChPs. White arrows indicate lipid positive areas. Data in a,b,c,e,h are representative images from at least 3 biologically independent mouse samples. Data in d,f,g represent means ± SEM; Two-tailed Student's t-test was applied to d,g; one-way ANOVA with Tukey posttest was applied to f; Gene names in .

Article Snippet: Immunofluorescence staining was performed as previously described , using marker antibodies anti-mouse collagen IV (2150-1470; AbDSerotec), immunoglobulins (715-166-151; Dianova), immunoglobulin isotype that do not react with mouse Ig (017-160-006; Dianova), anti-human/mouse C3 (A213, ComplementTech), anti-human/mouse C3a (A218, ComplementTech), anti-human C5 (A220, ComplementTech), anti-mouse C5 (ab11898, Abcam), isotype for C5 (ab27478, Abcam), anti-mouse C1q (HM1096BT, Hycult Biotech), anti-human C1q (ab71089, Abcam), anti-mouse C4 (HM1046, Hycult Biotech), anti-human Factor H (A312, Quidel), anti-mouse Factor H (HM1119F, Hycult Biotech), anti-human ApoE (ab52607, Abcam), anti-human ApoE (178479; Calbiochem), anti-mouse ApoE (ab183597, Abcam), anti-mouse CD68 (FA11; Serotec), anti-human CD68 (EMB11, DAKO), anti-mouse CD31 (553370; BD PharMingen), anti-mouse iba-1 (019-19741; WAKO), anti-mouse CD45 (BZL 01145; Biozol), anti-human/mouse cytokeratin (Z0622; DAKO), anti-human collagen IV (CIV22, DAKO), anti-beta-amyloid (4G8, Biolegend), anti-phospho-Tau (AT8, Thermofisher), anti-iba1 (polyclonal, WAKO), anti-LAMP1 (1D4B, Abcam), TO-PRO™-3 Iodide (642/661) (T3605, Thermo Fisher Scientific) or DAPI for DNA.

Techniques: Staining, Enzyme-linked Immunosorbent Assay, Confocal Microscopy, Two Tailed Test

( a ) ApoE isoforms bind to the C1 complex, but not to C4 or C2. Biotinylated ApoE was immobilized on streptavidin-coated sensors and incubated with C1 complex, C4, C2, or buffer; ( b ) The C1 complex binds to immobilized ApoE isoforms. ( c ) ApoE isoforms bind to C1 and factor H, but not to C3 or C3b; ( d ) Normal human serum (NHS)-derived C1 binds to immobilized plasma-purified ApoE3 and to recombinant ApoE isoforms; ( e ) C1q binds to immobilized plasma-purified ApoE3 and to all recombinant ApoE isoforms; ( f ) Plasma-purified C1q was coated on a sensor chip (CM5) and plasma-derived ApoE (62-1000 nM) was injected into the fluid phase (75 mM NaCl, 5 mM HEPES, 1 mM CaCl2). ( g ) Mannose-binding lectin (MBL) does not bind to C1q as determined by biolayer interferometry; ( h ) Apolipoprotein A (ApoA) does not bind to C1q as determined by biolayer interferometry. ( i ) C1q-ApoE complexes revealed by proximity ligation assay (PLA) on cultured human apoptotic cells (THP-1) were detectable when treated with NHS but not with C1q-depleted serum (dNHS). Data represent mean fluorescence intensity (MFI) ± SEM of 16 cells for each group. Bar 10 µm. Data in b,c,d,e represent means ± SEM of at least three independent experiments. Data a,f,g and h represent means of at least two independent experiments. Two-tailed Student's t-test.

Journal: Nature medicine

Article Title: ApoE attenuates unresolvable inflammation by complex formation with activated C1q

doi: 10.1038/s41591-018-0336-8

Figure Lengend Snippet: ( a ) ApoE isoforms bind to the C1 complex, but not to C4 or C2. Biotinylated ApoE was immobilized on streptavidin-coated sensors and incubated with C1 complex, C4, C2, or buffer; ( b ) The C1 complex binds to immobilized ApoE isoforms. ( c ) ApoE isoforms bind to C1 and factor H, but not to C3 or C3b; ( d ) Normal human serum (NHS)-derived C1 binds to immobilized plasma-purified ApoE3 and to recombinant ApoE isoforms; ( e ) C1q binds to immobilized plasma-purified ApoE3 and to all recombinant ApoE isoforms; ( f ) Plasma-purified C1q was coated on a sensor chip (CM5) and plasma-derived ApoE (62-1000 nM) was injected into the fluid phase (75 mM NaCl, 5 mM HEPES, 1 mM CaCl2). ( g ) Mannose-binding lectin (MBL) does not bind to C1q as determined by biolayer interferometry; ( h ) Apolipoprotein A (ApoA) does not bind to C1q as determined by biolayer interferometry. ( i ) C1q-ApoE complexes revealed by proximity ligation assay (PLA) on cultured human apoptotic cells (THP-1) were detectable when treated with NHS but not with C1q-depleted serum (dNHS). Data represent mean fluorescence intensity (MFI) ± SEM of 16 cells for each group. Bar 10 µm. Data in b,c,d,e represent means ± SEM of at least three independent experiments. Data a,f,g and h represent means of at least two independent experiments. Two-tailed Student's t-test.

Techniques: Incubation, Derivative Assay, Purification, Recombinant, Injection, Binding Assay, Proximity Ligation Assay, Cell Culture, Fluorescence, Two Tailed Test

( a - b ) Human ChP sections were stained for C1q (green) / C3 (red) ( a ) and C1q (green) / ApoE (red) ( b ); ( c - d) ChP sections were stained for CD68+ macrophages/DCs ( c ) and collagen IV (Col-IV) to mark basement membranes. Phase contrast shows lipid deposits in ChPs; ( e ) ChP sections were stained for ApoE (green) and factor H (red); no primary antibody as control (NA). ( f - g ) human brain sections were stained for Aβ (green) / ApoE (red) (left panels), Tau phosphorylation (pTau, green) / ApoE (red) (middle panels), and C1q (green) / ApoE (red) (right panels) (f). Blue for nuclei. No primary antibody as control ( g ); ( h ) brain parenchyma sections were stained for C3 (red) / ApoE (green). Bar 100 µm for a-h; Data in a-h are representative images from at least 3 biologically independent samples.

Journal: Nature medicine

Article Title: ApoE attenuates unresolvable inflammation by complex formation with activated C1q

doi: 10.1038/s41591-018-0336-8

Figure Lengend Snippet: ( a - b ) Human ChP sections were stained for C1q (green) / C3 (red) ( a ) and C1q (green) / ApoE (red) ( b ); ( c - d) ChP sections were stained for CD68+ macrophages/DCs ( c ) and collagen IV (Col-IV) to mark basement membranes. Phase contrast shows lipid deposits in ChPs; ( e ) ChP sections were stained for ApoE (green) and factor H (red); no primary antibody as control (NA). ( f - g ) human brain sections were stained for Aβ (green) / ApoE (red) (left panels), Tau phosphorylation (pTau, green) / ApoE (red) (middle panels), and C1q (green) / ApoE (red) (right panels) (f). Blue for nuclei. No primary antibody as control ( g ); ( h ) brain parenchyma sections were stained for C3 (red) / ApoE (green). Bar 100 µm for a-h; Data in a-h are representative images from at least 3 biologically independent samples.

Techniques: Staining

( a ) Expression microarray analyses of aortas. Heatmaps
show GO terms leukocyte migration, complement activation, phagocytosis, and
cellular response to lipid. 6 weeks WT (n=3 mice); 32 weeks WT (n=3); 6
weeks ApoE-/- (n=3); 32 weeks ApoE-/- (n=3); ( b ) aorta
alternative complement pathway genes (factor B, factor H, factor D) mRNA
expression in 6 weeks and 32 weeks old WT and ApoE-/- mouse aortas. 6 weeks
WT (n=3 mice); 32 weeks WT (n=3); 6 weeks ApoE-/- (n=3); 32 weeks ApoE-/-
(n=3); ( c - d ) plasma cholesterol and body weight;
( e - f ) blood leukocytes and percentage. For
c-f, control (11 mice); C5 siRNA (12 mice). ( g ) blood CD4+ T
cells, CD8+ T cells, and B220+ B cells by flow cytometry. Control (6 mice);
C5 siRNA (6 mice). ( h ) super-resolution microscopy shows
colocalization of C1q (green) and ApoE (red) in human atherosclerotic
plaque. Representative images from at least 3 biologically independent mouse
samples. Bar 5 µm. Data in b,c,d,e,f,g represent means ± SEM;
Two-tailed Student's t-test was applied to c.d.e.f.g; one-way ANOVA with
Tukey posttest was applied to b; abbreviations: WBC, white blood cells; RBC,
red blood cells; PLT, platelets; LYM, lymphocytes; MO, monocytes; GRA,
granulocytes. Gene names and statistics in .

Journal: Nature medicine

Article Title: ApoE attenuates unresolvable inflammation by complex formation with activated C1q

doi: 10.1038/s41591-018-0336-8

Figure Lengend Snippet: ( a ) Expression microarray analyses of aortas. Heatmaps show GO terms leukocyte migration, complement activation, phagocytosis, and cellular response to lipid. 6 weeks WT (n=3 mice); 32 weeks WT (n=3); 6 weeks ApoE-/- (n=3); 32 weeks ApoE-/- (n=3); ( b ) aorta alternative complement pathway genes (factor B, factor H, factor D) mRNA expression in 6 weeks and 32 weeks old WT and ApoE-/- mouse aortas. 6 weeks WT (n=3 mice); 32 weeks WT (n=3); 6 weeks ApoE-/- (n=3); 32 weeks ApoE-/- (n=3); ( c - d ) plasma cholesterol and body weight; ( e - f ) blood leukocytes and percentage. For c-f, control (11 mice); C5 siRNA (12 mice). ( g ) blood CD4+ T cells, CD8+ T cells, and B220+ B cells by flow cytometry. Control (6 mice); C5 siRNA (6 mice). ( h ) super-resolution microscopy shows colocalization of C1q (green) and ApoE (red) in human atherosclerotic plaque. Representative images from at least 3 biologically independent mouse samples. Bar 5 µm. Data in b,c,d,e,f,g represent means ± SEM; Two-tailed Student's t-test was applied to c.d.e.f.g; one-way ANOVA with Tukey posttest was applied to b; abbreviations: WBC, white blood cells; RBC, red blood cells; PLT, platelets; LYM, lymphocytes; MO, monocytes; GRA, granulocytes. Gene names and statistics in .

Techniques: Expressing, Microarray, Migration, Activation Assay, Flow Cytometry, Microscopy, Two Tailed Test

( A ) The depicted constructs were used to generate transgenic animals that expressed human C4BP and/or FH in addition to their endogenous counterpart C4BP and FH molecules. ( B ) PCR analysis confirmed the presence of the either hu-C4BP α-chains (upper panel), human Factor H (FH) (lower panel) or both (both panels) in the tg animals, but not in BALB/c wt mice. (C) SDS-PAGE and western blot analysis confirmed that hu-C4BP ( C , upper panel non-reduced gel) and hu-FH ( C , lower panel, reduced gel) were detectable in the appropriately designated tg, but not in BALB/c mouse serum. ( D ) Serum levels of hu-C4BP and hu-FH were determined using a sandwich-ELISA. ( E) BALB/c (blue) and hu-C4BPxFH tg (red) serum (20%) deposit similar amounts of C3 on zymosan particles by flow cytometry. EDTA-treated BALB/c serum (negative control) did not deposit any C3 on zymosan (negative control; n = 3 sera from individual animals). Statistical analysis: Kruskal-Wallis analysis with Dunn’s post-test ( D ) and 1-way ANOVA with Bonferroni’s post-test ( E ).

Journal: PLoS Pathogens

Article Title: Virulence of Group A Streptococci Is Enhanced by Human Complement Inhibitors

doi: 10.1371/journal.ppat.1005043

Figure Lengend Snippet: ( A ) The depicted constructs were used to generate transgenic animals that expressed human C4BP and/or FH in addition to their endogenous counterpart C4BP and FH molecules. ( B ) PCR analysis confirmed the presence of the either hu-C4BP α-chains (upper panel), human Factor H (FH) (lower panel) or both (both panels) in the tg animals, but not in BALB/c wt mice. (C) SDS-PAGE and western blot analysis confirmed that hu-C4BP ( C , upper panel non-reduced gel) and hu-FH ( C , lower panel, reduced gel) were detectable in the appropriately designated tg, but not in BALB/c mouse serum. ( D ) Serum levels of hu-C4BP and hu-FH were determined using a sandwich-ELISA. ( E) BALB/c (blue) and hu-C4BPxFH tg (red) serum (20%) deposit similar amounts of C3 on zymosan particles by flow cytometry. EDTA-treated BALB/c serum (negative control) did not deposit any C3 on zymosan (negative control; n = 3 sera from individual animals). Statistical analysis: Kruskal-Wallis analysis with Dunn’s post-test ( D ) and 1-way ANOVA with Bonferroni’s post-test ( E ).

Article Snippet: For flow cytometry analysis, the following antibodies were used: mouse anti human-C4BP MK104 either unconjugated or conjugated to biotin; mouse anti human-Factor H MRC OX24 unconjugated or conjugated to biotin; rabbit anti mouse-C4BP (homemade) conjugated to Dylight 647; mouse monoclonal anti mouse-Factor H (Hycult, HM1119) conjugated to biotin; goat anti mouse-C3c (Nordic Immunology, GAM/C3c/7S); anti mouse C3 FITC (MP Biomedicals #0855500) anti mouse Ly-6G brilliant violet 421 (BioLegend, #127627); anti mouse Ly-6C PerCP/Cy5.5 (BioLegend, #128011); anti mouse CD11c (BioLegend, #117317); anti mouse I-A/I-E brilliant violet 510 (BioLegend, #107635); anti mouse CD64 APC (BioLegend, #139305); anti mouse/human CD11b APC/Cy7 (BioLegend, #101225).

Techniques: Construct, Transgenic Assay, SDS Page, Western Blot, Sandwich ELISA, Flow Cytometry, Negative Control

Review

Structured Review

Images

Similar Products

Image Search Results