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R&D Systems mouse anti human gip

Cellular responses to <t>GIP_HUMAN[22–51].</t> ( a, b ) Confocal laser-scanning microscopy images of the fluorescent GIP_HUMAN[22–51] peptides bound to cultured cells. Growing HAoECs ( a ) or THP1-derived macrophages deprived of serum for 16 h ( b ) were overlaid without (left panels) or with 10 –6 M FAM-GIP_HUMAN[22–51] (right panels) for 30 or 5 min, respectively. Cells were washed, fixed, nuclei counterstained with DAPI (blue) and the cell surface-bound green fluorescence visualised. Scale bar represents 50 μm. ( c, d ) Nuclear translocation of NF-κB. HAoECs ( c ) or THP1-derived macrophages ( d ) were incubated without (left panel) or with 10 –6 M GIP_HUMAN[22–51] for 60 min, and immunocytochemical staining was performed using an NF-κB p65 subunit antibody to detect its nuclear translocation. ( e, f ) Degradation of IκB-α. HAoECs ( e ) or THP1-derived macrophages ( f ) were stimulated with 10 –7 M GIP_HUMAN[22–51] for the indicated times and subjected to western blot analysis using the anti-IκB-α antibody to assess the time-course of IκB-α degradation. The panels show the cropped blots and the full-length blots are presented in the Supplementary Information. ( g–i ) Upregulation of MMP8 gene expression by GIP_HUMAN[22–51]. HAoECs were incubated with 10 –7 M GIP_HUMAN[22–51] for the indicated times ( g ) or with indicated doses for 48 h ( h ), and MMP8 mRNA and β-actin levels were quantified. Data represent the fold changes (mean ± S.E.M) of MMP8 mRNA copies relative to β-actin mRNA ( n = 5). * p < 0.05, ** p < 0.01, *** p < 0.001 compared with vehicle. ( i ) HAoECs pre-treated with or without MG132 (500 nM) for 30 min were incubated with 10 –7 M GIP_HUMAN[22–51] and MG132 (100 nM) for 24 h and MMP8 and β-actin mRNA levels were quantified. ** p < 0.01, *** p < 0.001, compared with vehicle. The relative mRNA levels are shown as fold changes (mean ± S.E.M; n = 5).

Mouse Anti Human Gip, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "GIP_HUMAN[22–51] is a new proatherogenic peptide identified by native plasma peptidomics"

Article Title: GIP_HUMAN[22–51] is a new proatherogenic peptide identified by native plasma peptidomics

Journal: Scientific Reports

doi: 10.1038/s41598-021-93862-w

Cellular responses to GIP_HUMAN[22–51]. ( a, b ) Confocal laser-scanning microscopy images of the fluorescent GIP_HUMAN[22–51] peptides bound to cultured cells. Growing HAoECs ( a ) or THP1-derived macrophages deprived of serum for 16 h ( b ) were overlaid without (left panels) or with 10 –6 M FAM-GIP_HUMAN[22–51] (right panels) for 30 or 5 min, respectively. Cells were washed, fixed, nuclei counterstained with DAPI (blue) and the cell surface-bound green fluorescence visualised. Scale bar represents 50 μm. ( c, d ) Nuclear translocation of NF-κB. HAoECs ( c ) or THP1-derived macrophages ( d ) were incubated without (left panel) or with 10 –6 M GIP_HUMAN[22–51] for 60 min, and immunocytochemical staining was performed using an NF-κB p65 subunit antibody to detect its nuclear translocation. ( e, f ) Degradation of IκB-α. HAoECs ( e ) or THP1-derived macrophages ( f ) were stimulated with 10 –7 M GIP_HUMAN[22–51] for the indicated times and subjected to western blot analysis using the anti-IκB-α antibody to assess the time-course of IκB-α degradation. The panels show the cropped blots and the full-length blots are presented in the Supplementary Information. ( g–i ) Upregulation of MMP8 gene expression by GIP_HUMAN[22–51]. HAoECs were incubated with 10 –7 M GIP_HUMAN[22–51] for the indicated times ( g ) or with indicated doses for 48 h ( h ), and MMP8 mRNA and β-actin levels were quantified. Data represent the fold changes (mean ± S.E.M) of MMP8 mRNA copies relative to β-actin mRNA ( n = 5). * p < 0.05, ** p < 0.01, *** p < 0.001 compared with vehicle. ( i ) HAoECs pre-treated with or without MG132 (500 nM) for 30 min were incubated with 10 –7 M GIP_HUMAN[22–51] and MG132 (100 nM) for 24 h and MMP8 and β-actin mRNA levels were quantified. ** p < 0.01, *** p < 0.001, compared with vehicle. The relative mRNA levels are shown as fold changes (mean ± S.E.M; n = 5).

Figure Legend Snippet: Cellular responses to GIP_HUMAN[22–51]. ( a, b ) Confocal laser-scanning microscopy images of the fluorescent GIP_HUMAN[22–51] peptides bound to cultured cells. Growing HAoECs ( a ) or THP1-derived macrophages deprived of serum for 16 h ( b ) were overlaid without (left panels) or with 10 –6 M FAM-GIP_HUMAN[22–51] (right panels) for 30 or 5 min, respectively. Cells were washed, fixed, nuclei counterstained with DAPI (blue) and the cell surface-bound green fluorescence visualised. Scale bar represents 50 μm. ( c, d ) Nuclear translocation of NF-κB. HAoECs ( c ) or THP1-derived macrophages ( d ) were incubated without (left panel) or with 10 –6 M GIP_HUMAN[22–51] for 60 min, and immunocytochemical staining was performed using an NF-κB p65 subunit antibody to detect its nuclear translocation. ( e, f ) Degradation of IκB-α. HAoECs ( e ) or THP1-derived macrophages ( f ) were stimulated with 10 –7 M GIP_HUMAN[22–51] for the indicated times and subjected to western blot analysis using the anti-IκB-α antibody to assess the time-course of IκB-α degradation. The panels show the cropped blots and the full-length blots are presented in the Supplementary Information. ( g–i ) Upregulation of MMP8 gene expression by GIP_HUMAN[22–51]. HAoECs were incubated with 10 –7 M GIP_HUMAN[22–51] for the indicated times ( g ) or with indicated doses for 48 h ( h ), and MMP8 mRNA and β-actin levels were quantified. Data represent the fold changes (mean ± S.E.M) of MMP8 mRNA copies relative to β-actin mRNA ( n = 5). * p < 0.05, ** p < 0.01, *** p < 0.001 compared with vehicle. ( i ) HAoECs pre-treated with or without MG132 (500 nM) for 30 min were incubated with 10 –7 M GIP_HUMAN[22–51] and MG132 (100 nM) for 24 h and MMP8 and β-actin mRNA levels were quantified. ** p < 0.01, *** p < 0.001, compared with vehicle. The relative mRNA levels are shown as fold changes (mean ± S.E.M; n = 5).

Techniques Used: Confocal Laser Scanning Microscopy, Cell Culture, Derivative Assay, Fluorescence, Translocation Assay, Incubation, Staining, Western Blot, Expressing

Proatherosclerotic effects of GIP_HUMAN[22–51] in ApoE −/− mice. The 17-week-old ApoE −/− mice were infused with saline alone ( a , e, and i , vehicle), GIP_HUMAN[22–51] ( b , c , f , g , j, and k , 0.6 nM/kg/h), and/or anti-GIP_HUMAN[22–51] IgG ( c , d , g , h , k, and l , 1.4 μg/kg/h) by osmotic mini-pumps for 4 weeks. The aortic surface was stained with oil red O ( a – d ). Cross sections of the aortic root were stained with oil red O ( e – h ) or anti-MOMA-2 antibody ( i – l ) and counterstained with hematoxylin. Surface area of the atherosclerotic lesions ( m ), cross sectional area of the atherosclerotic lesion ( n ), and macrophage accumulation ( o ) are expressed as means ± SEM ( n = 5–7). * p < 0.05, ** p < 0.01, *** p < 0.001 compared with vehicle.

Figure Legend Snippet: Proatherosclerotic effects of GIP_HUMAN[22–51] in ApoE −/− mice. The 17-week-old ApoE −/− mice were infused with saline alone ( a , e, and i , vehicle), GIP_HUMAN[22–51] ( b , c , f , g , j, and k , 0.6 nM/kg/h), and/or anti-GIP_HUMAN[22–51] IgG ( c , d , g , h , k, and l , 1.4 μg/kg/h) by osmotic mini-pumps for 4 weeks. The aortic surface was stained with oil red O ( a – d ). Cross sections of the aortic root were stained with oil red O ( e – h ) or anti-MOMA-2 antibody ( i – l ) and counterstained with hematoxylin. Surface area of the atherosclerotic lesions ( m ), cross sectional area of the atherosclerotic lesion ( n ), and macrophage accumulation ( o ) are expressed as means ± SEM ( n = 5–7). * p < 0.05, ** p < 0.01, *** p < 0.001 compared with vehicle.

Techniques Used: Saline, Staining

Cytokine array screening of mice serum infused with GIP_HUMAN[22–51] for 4 weeks. ( a ) Layout of antibody arrays and abbreviated names of the 111 cytokine/chemokine probes, adapted from the manufacturer’s information. ( b – e ) Complete hybridisation signals after probing with serum samples obtained from ApoE−/− mice infused for 4 weeks with saline alone ( b ), GIP_HUMAN[22–51] ( c ), combined infusion with GIP_HUMAN[22–51] and anti-GIP_HUMAN[22–51] IgG ( d ), or anti-GIP_HUMAN[22–51] IgG ( e ). ( f , g ) Quantified signal intensities of the respective serum proteins in mice infused with GIP_HUMAN[22–51] ( f ) or anti-GIP_HUMAN[22–51] IgG ( g ) in terms of 2-spot mean values relative to untreated experiments are shown.

Figure Legend Snippet: Cytokine array screening of mice serum infused with GIP_HUMAN[22–51] for 4 weeks. ( a ) Layout of antibody arrays and abbreviated names of the 111 cytokine/chemokine probes, adapted from the manufacturer’s information. ( b – e ) Complete hybridisation signals after probing with serum samples obtained from ApoE−/− mice infused for 4 weeks with saline alone ( b ), GIP_HUMAN[22–51] ( c ), combined infusion with GIP_HUMAN[22–51] and anti-GIP_HUMAN[22–51] IgG ( d ), or anti-GIP_HUMAN[22–51] IgG ( e ). ( f , g ) Quantified signal intensities of the respective serum proteins in mice infused with GIP_HUMAN[22–51] ( f ) or anti-GIP_HUMAN[22–51] IgG ( g ) in terms of 2-spot mean values relative to untreated experiments are shown.

Techniques Used: Hybridization, Saline

Systemic expression of GIP_HUMAN[22–51] and its negative colocalisation with GIP in major human organs. ( a–l , a ’– l ’) Human tissue array sections were immunohistochemically stained with either IgG purified from preimmune rabbit serum ( a–l ) or anti-GIP_HUMAN[22–51] IgG at 1:500 dilution ( a ’– l ’). Arrows indicate the positions of positive immunoreactivity. ( a” – l” ) Confocal microscopic images of immunofluorescent dual staining of GIP_HUMAN[22–51] and GIP. Human tissue array sections were double-stained with either the rabbit polyclonal anti-GIP_HUMAN[22–51] antibody (× 1000) or the mouse monoclonal anti-human GIP antibody (× 500). The red signals corresponding to the localisation of GIP were obtained with the Alexa Fluor 594 secondary antibody (× 1000) and the green signals representing GIP_HUMAN[22–51] were obtained with the Alexa Fluor 488 secondary antibody (× 500). The nuclei were counterstained with DAPI (blue). Overlay resulted in yellow signals indicative of colocalisation. ( a–a” ) cerebral cortex, ( b – b ”) cerebellum, ( c – c ”) tonsil, ( d – d ”) lymph node, ( e – e ”) heart, ( f – f ”) liver, ( g – g ”) stomach, ( h – h ”) kidney (glomerulus), ( i – i ”) kidney (tubule), ( j – j ”) small intestine, ( k – k ”) colon and ( l – l ”) testis (scale bar: 100 μm).

Figure Legend Snippet: Systemic expression of GIP_HUMAN[22–51] and its negative colocalisation with GIP in major human organs. ( a–l , a ’– l ’) Human tissue array sections were immunohistochemically stained with either IgG purified from preimmune rabbit serum ( a–l ) or anti-GIP_HUMAN[22–51] IgG at 1:500 dilution ( a ’– l ’). Arrows indicate the positions of positive immunoreactivity. ( a” – l” ) Confocal microscopic images of immunofluorescent dual staining of GIP_HUMAN[22–51] and GIP. Human tissue array sections were double-stained with either the rabbit polyclonal anti-GIP_HUMAN[22–51] antibody (× 1000) or the mouse monoclonal anti-human GIP antibody (× 500). The red signals corresponding to the localisation of GIP were obtained with the Alexa Fluor 594 secondary antibody (× 1000) and the green signals representing GIP_HUMAN[22–51] were obtained with the Alexa Fluor 488 secondary antibody (× 500). The nuclei were counterstained with DAPI (blue). Overlay resulted in yellow signals indicative of colocalisation. ( a–a” ) cerebral cortex, ( b – b ”) cerebellum, ( c – c ”) tonsil, ( d – d ”) lymph node, ( e – e ”) heart, ( f – f ”) liver, ( g – g ”) stomach, ( h – h ”) kidney (glomerulus), ( i – i ”) kidney (tubule), ( j – j ”) small intestine, ( k – k ”) colon and ( l – l ”) testis (scale bar: 100 μm).

Techniques Used: Expressing, Staining, Purification

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Journal: Scientific Reports

Article Title: GIP_HUMAN[22–51] is a new proatherogenic peptide identified by native plasma peptidomics

doi: 10.1038/s41598-021-93862-w

Figure Lengend Snippet: Cellular responses to GIP_HUMAN[22–51]. ( a, b ) Confocal laser-scanning microscopy images of the fluorescent GIP_HUMAN[22–51] peptides bound to cultured cells. Growing HAoECs ( a ) or THP1-derived macrophages deprived of serum for 16 h ( b ) were overlaid without (left panels) or with 10 –6 M FAM-GIP_HUMAN[22–51] (right panels) for 30 or 5 min, respectively. Cells were washed, fixed, nuclei counterstained with DAPI (blue) and the cell surface-bound green fluorescence visualised. Scale bar represents 50 μm. ( c, d ) Nuclear translocation of NF-κB. HAoECs ( c ) or THP1-derived macrophages ( d ) were incubated without (left panel) or with 10 –6 M GIP_HUMAN[22–51] for 60 min, and immunocytochemical staining was performed using an NF-κB p65 subunit antibody to detect its nuclear translocation. ( e, f ) Degradation of IκB-α. HAoECs ( e ) or THP1-derived macrophages ( f ) were stimulated with 10 –7 M GIP_HUMAN[22–51] for the indicated times and subjected to western blot analysis using the anti-IκB-α antibody to assess the time-course of IκB-α degradation. The panels show the cropped blots and the full-length blots are presented in the Supplementary Information. ( g–i ) Upregulation of MMP8 gene expression by GIP_HUMAN[22–51]. HAoECs were incubated with 10 –7 M GIP_HUMAN[22–51] for the indicated times ( g ) or with indicated doses for 48 h ( h ), and MMP8 mRNA and β-actin levels were quantified. Data represent the fold changes (mean ± S.E.M) of MMP8 mRNA copies relative to β-actin mRNA ( n = 5). * p < 0.05, ** p < 0.01, *** p < 0.001 compared with vehicle. ( i ) HAoECs pre-treated with or without MG132 (500 nM) for 30 min were incubated with 10 –7 M GIP_HUMAN[22–51] and MG132 (100 nM) for 24 h and MMP8 and β-actin mRNA levels were quantified. ** p < 0.01, *** p < 0.001, compared with vehicle. The relative mRNA levels are shown as fold changes (mean ± S.E.M; n = 5).

Article Snippet: For the comparison of the exact expression sites of GIP_HUMAN[22–51] and the mature GIP using dual immunofluorescence staining, we followed the same procedures as described for normal immunohistochemical staining with tissue array, MNO341, except that we used two primary antibodies, the rabbit anti- GIP_HUMAN[22–51] IgG (1:1000) and the mouse anti-human GIP (1:500, R&D Systems) simultaneously, and two secondary antibodies, the goat anti-rabbit-Alexa Fluor 488-conjugated antibody (1:500, Abcam) and the goat anti-mouse-Alexa Fluor 594-conjugated antibody (1:1000, Abcam).

Techniques: Confocal Laser Scanning Microscopy, Cell Culture, Derivative Assay, Fluorescence, Translocation Assay, Incubation, Staining, Western Blot, Expressing

Journal: Scientific Reports

Article Title: GIP_HUMAN[22–51] is a new proatherogenic peptide identified by native plasma peptidomics

doi: 10.1038/s41598-021-93862-w

Figure Lengend Snippet: Proatherosclerotic effects of GIP_HUMAN[22–51] in ApoE −/− mice. The 17-week-old ApoE −/− mice were infused with saline alone ( a , e, and i , vehicle), GIP_HUMAN[22–51] ( b , c , f , g , j, and k , 0.6 nM/kg/h), and/or anti-GIP_HUMAN[22–51] IgG ( c , d , g , h , k, and l , 1.4 μg/kg/h) by osmotic mini-pumps for 4 weeks. The aortic surface was stained with oil red O ( a – d ). Cross sections of the aortic root were stained with oil red O ( e – h ) or anti-MOMA-2 antibody ( i – l ) and counterstained with hematoxylin. Surface area of the atherosclerotic lesions ( m ), cross sectional area of the atherosclerotic lesion ( n ), and macrophage accumulation ( o ) are expressed as means ± SEM ( n = 5–7). * p < 0.05, ** p < 0.01, *** p < 0.001 compared with vehicle.

Techniques: Saline, Staining

Journal: Scientific Reports

Article Title: GIP_HUMAN[22–51] is a new proatherogenic peptide identified by native plasma peptidomics

doi: 10.1038/s41598-021-93862-w

Figure Lengend Snippet: Cytokine array screening of mice serum infused with GIP_HUMAN[22–51] for 4 weeks. ( a ) Layout of antibody arrays and abbreviated names of the 111 cytokine/chemokine probes, adapted from the manufacturer’s information. ( b – e ) Complete hybridisation signals after probing with serum samples obtained from ApoE−/− mice infused for 4 weeks with saline alone ( b ), GIP_HUMAN[22–51] ( c ), combined infusion with GIP_HUMAN[22–51] and anti-GIP_HUMAN[22–51] IgG ( d ), or anti-GIP_HUMAN[22–51] IgG ( e ). ( f , g ) Quantified signal intensities of the respective serum proteins in mice infused with GIP_HUMAN[22–51] ( f ) or anti-GIP_HUMAN[22–51] IgG ( g ) in terms of 2-spot mean values relative to untreated experiments are shown.

Techniques: Hybridization, Saline

Journal: Scientific Reports

Article Title: GIP_HUMAN[22–51] is a new proatherogenic peptide identified by native plasma peptidomics

doi: 10.1038/s41598-021-93862-w

Figure Lengend Snippet: Systemic expression of GIP_HUMAN[22–51] and its negative colocalisation with GIP in major human organs. ( a–l , a ’– l ’) Human tissue array sections were immunohistochemically stained with either IgG purified from preimmune rabbit serum ( a–l ) or anti-GIP_HUMAN[22–51] IgG at 1:500 dilution ( a ’– l ’). Arrows indicate the positions of positive immunoreactivity. ( a” – l” ) Confocal microscopic images of immunofluorescent dual staining of GIP_HUMAN[22–51] and GIP. Human tissue array sections were double-stained with either the rabbit polyclonal anti-GIP_HUMAN[22–51] antibody (× 1000) or the mouse monoclonal anti-human GIP antibody (× 500). The red signals corresponding to the localisation of GIP were obtained with the Alexa Fluor 594 secondary antibody (× 1000) and the green signals representing GIP_HUMAN[22–51] were obtained with the Alexa Fluor 488 secondary antibody (× 500). The nuclei were counterstained with DAPI (blue). Overlay resulted in yellow signals indicative of colocalisation. ( a–a” ) cerebral cortex, ( b – b ”) cerebellum, ( c – c ”) tonsil, ( d – d ”) lymph node, ( e – e ”) heart, ( f – f ”) liver, ( g – g ”) stomach, ( h – h ”) kidney (glomerulus), ( i – i ”) kidney (tubule), ( j – j ”) small intestine, ( k – k ”) colon and ( l – l ”) testis (scale bar: 100 μm).

Techniques: Expressing, Staining, Purification

Densities of enteroendocrine cells in the duodenum of controls, total IBS group, PI-IBS, and idiopathic IBS patients before and after receiving FMT.

Journal: Frontiers in Cellular and Infection Microbiology

Article Title: The Effects of Fecal Microbiota Transplantation on the Symptoms and the Duodenal Neurogenin 3, Musashi 1, and Enteroendocrine Cells in Patients With Diarrhea-Predominant Irritable Bowel Syndrome

doi: 10.3389/fcimb.2021.524851

Figure Lengend Snippet: Densities of enteroendocrine cells in the duodenum of controls, total IBS group, PI-IBS, and idiopathic IBS patients before and after receiving FMT.

Article Snippet: The primary antibodies that were diluted according to the suppliers’ recommendations were as follows: polyclonal rabbit anti-synthetic peptide conjugated to keyhole limpet hemocyanin derived from within residues 1–100 of human Msi-1 (code ab21628, Abcam, Cambridge, United Kingdom), monoclonal mouse-anti-protein expressed in 293T cells transfected with human NEUROG3 expression vector (code ab87108, Abcam), monoclonal mouse antibody raised against the N-terminal of purified CgA (code no. M869, Dako, Glostrup, Denmark), polyclonal rabbit anti-human secretin for the detection of secretin (code no. sc-20938, Santa Cruz Biotechnology, Santa Cruz, CA, United States), rabbit antibodies for the detection of cholecystokinin (CCK; code no. A0568, Dako, Glostrup, Denmark), mouse antibodies against human synthetic gastric inhibitory peptide (GIP; code no. sc-57162, Santa Cruz Biotechnology), mouse antibodies against serotonin (code no. R87104 B56-1, Dako), and rabbit antibodies against synthetic cyclic somatostatin (code no. A0566, Dako).

Techniques: Control

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