mouse ril-33 Search Results


mouse ril-33  (Adipogen)
90
Adipogen mouse ril-33
The Il33 gene is completely deleted in the mutant mice and recombinant IL-33 protein restored insulin resistance in the muscle of the preobese mutant mice. ( A ) Schematic representation of the control and mutant allele surrounding the transgene integration site. Transgene integration caused the deletion of a 124.2-kb genomic DNA fragment (a blue region) at the left integration (LI) site of the mutant allele. It also caused the inversion of a 38.2-kb genomic DNA fragment with one break in the right breakpoint (RB) and the other break in the right transgene integration (RI) site (a red arrow) and the deletion of a 4.6-kb DNA fragment (a yellow region) at the right end of the mutant allele. The orientation of transcription is indicated by black arrows. White arrowheads indicate PCR primers (a1 and a3, b1-b3, and c1-c3) used for confirmation of the transgene insertion sites and breakpoint region. The orientation of the genomic DNA with respect to the centromere (cen) and telomere (tel) of chromosome 19 is indicated by black arrowheads. Flp, Flp recombinase expression vector pEF-NFLP. ( B ) PCR analysis of genomic DNA from the control and mutant mice using primers based on the inserted transgene and the flanking endogenous genomic DNA (left and center panels) or the flanking right breakpoint (right panel). Lane M contains size markers. ( C ) Real-time quantitative RT-PCR analysis in the various tissue of the control (white bars) and preobese mutant (mint green bars) mice (n = 7-10 per group). n.d., not detectable. ( D ) Insulin tolerance test (0.75 mU/g of body weight) results of the male control (white circles), the preobese mutant (mint green circles) and recombinant IL-33 <t>(rIL-33)</t> protein treated preobese mutant (light blue triangles) mice (n = 8-9 per group). The preobese mutant mice received an intraperitoneal injection of vehicle or rIL-33 at 1 hour before the insulin tolerance test. The control versus preobese mutant mice with vehicle: *P < 0.05, **P < 0.01; Vehicle versus rIL-33 treated preobese mutant mice: †P < 0.05, ††P < 0.01. ( E ), GIR (left), EGP (center), and R d (right) of the male control (white bars), preobese mutant (mint green bars) and rIL-33 treated preobese mutant (light blue bars) mice in the hyperinsulinemic-euglycemic clamp studies (n = 6-12 per group). *P < 0.05; **P < 0.01; n.s., not significant. ( F ) Real-time quantitative RT-PCR analysis in the muscle (left) and the liver (right) of the control (white bars) and preobese mutant (mint green bars) mice (n = 7-10 per group). n.d., not detectable. Means ± SEM.
Mouse Ril 33, supplied by Adipogen, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mouse ril-33/product/Adipogen
Average 90 stars, based on 1 article reviews
mouse ril-33 - by Bioz Stars, 2026-03
90/100 stars
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full-length mouse il-33  (Cowin Biosciences)
90
Cowin Biosciences full-length mouse il-33
The Il33 gene is completely deleted in the mutant mice and recombinant IL-33 protein restored insulin resistance in the muscle of the preobese mutant mice. ( A ) Schematic representation of the control and mutant allele surrounding the transgene integration site. Transgene integration caused the deletion of a 124.2-kb genomic DNA fragment (a blue region) at the left integration (LI) site of the mutant allele. It also caused the inversion of a 38.2-kb genomic DNA fragment with one break in the right breakpoint (RB) and the other break in the right transgene integration (RI) site (a red arrow) and the deletion of a 4.6-kb DNA fragment (a yellow region) at the right end of the mutant allele. The orientation of transcription is indicated by black arrows. White arrowheads indicate PCR primers (a1 and a3, b1-b3, and c1-c3) used for confirmation of the transgene insertion sites and breakpoint region. The orientation of the genomic DNA with respect to the centromere (cen) and telomere (tel) of chromosome 19 is indicated by black arrowheads. Flp, Flp recombinase expression vector pEF-NFLP. ( B ) PCR analysis of genomic DNA from the control and mutant mice using primers based on the inserted transgene and the flanking endogenous genomic DNA (left and center panels) or the flanking right breakpoint (right panel). Lane M contains size markers. ( C ) Real-time quantitative RT-PCR analysis in the various tissue of the control (white bars) and preobese mutant (mint green bars) mice (n = 7-10 per group). n.d., not detectable. ( D ) Insulin tolerance test (0.75 mU/g of body weight) results of the male control (white circles), the preobese mutant (mint green circles) and recombinant IL-33 <t>(rIL-33)</t> protein treated preobese mutant (light blue triangles) mice (n = 8-9 per group). The preobese mutant mice received an intraperitoneal injection of vehicle or rIL-33 at 1 hour before the insulin tolerance test. The control versus preobese mutant mice with vehicle: *P < 0.05, **P < 0.01; Vehicle versus rIL-33 treated preobese mutant mice: †P < 0.05, ††P < 0.01. ( E ), GIR (left), EGP (center), and R d (right) of the male control (white bars), preobese mutant (mint green bars) and rIL-33 treated preobese mutant (light blue bars) mice in the hyperinsulinemic-euglycemic clamp studies (n = 6-12 per group). *P < 0.05; **P < 0.01; n.s., not significant. ( F ) Real-time quantitative RT-PCR analysis in the muscle (left) and the liver (right) of the control (white bars) and preobese mutant (mint green bars) mice (n = 7-10 per group). n.d., not detectable. Means ± SEM.
Full Length Mouse Il 33, supplied by Cowin Biosciences, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/full-length mouse il-33/product/Cowin Biosciences
Average 90 stars, based on 1 article reviews
full-length mouse il-33 - by Bioz Stars, 2026-03
90/100 stars
  Buy from Supplier

Image Search Results


The Il33 gene is completely deleted in the mutant mice and recombinant IL-33 protein restored insulin resistance in the muscle of the preobese mutant mice. ( A ) Schematic representation of the control and mutant allele surrounding the transgene integration site. Transgene integration caused the deletion of a 124.2-kb genomic DNA fragment (a blue region) at the left integration (LI) site of the mutant allele. It also caused the inversion of a 38.2-kb genomic DNA fragment with one break in the right breakpoint (RB) and the other break in the right transgene integration (RI) site (a red arrow) and the deletion of a 4.6-kb DNA fragment (a yellow region) at the right end of the mutant allele. The orientation of transcription is indicated by black arrows. White arrowheads indicate PCR primers (a1 and a3, b1-b3, and c1-c3) used for confirmation of the transgene insertion sites and breakpoint region. The orientation of the genomic DNA with respect to the centromere (cen) and telomere (tel) of chromosome 19 is indicated by black arrowheads. Flp, Flp recombinase expression vector pEF-NFLP. ( B ) PCR analysis of genomic DNA from the control and mutant mice using primers based on the inserted transgene and the flanking endogenous genomic DNA (left and center panels) or the flanking right breakpoint (right panel). Lane M contains size markers. ( C ) Real-time quantitative RT-PCR analysis in the various tissue of the control (white bars) and preobese mutant (mint green bars) mice (n = 7-10 per group). n.d., not detectable. ( D ) Insulin tolerance test (0.75 mU/g of body weight) results of the male control (white circles), the preobese mutant (mint green circles) and recombinant IL-33 (rIL-33) protein treated preobese mutant (light blue triangles) mice (n = 8-9 per group). The preobese mutant mice received an intraperitoneal injection of vehicle or rIL-33 at 1 hour before the insulin tolerance test. The control versus preobese mutant mice with vehicle: *P < 0.05, **P < 0.01; Vehicle versus rIL-33 treated preobese mutant mice: †P < 0.05, ††P < 0.01. ( E ), GIR (left), EGP (center), and R d (right) of the male control (white bars), preobese mutant (mint green bars) and rIL-33 treated preobese mutant (light blue bars) mice in the hyperinsulinemic-euglycemic clamp studies (n = 6-12 per group). *P < 0.05; **P < 0.01; n.s., not significant. ( F ) Real-time quantitative RT-PCR analysis in the muscle (left) and the liver (right) of the control (white bars) and preobese mutant (mint green bars) mice (n = 7-10 per group). n.d., not detectable. Means ± SEM.

Journal: bioRxiv

Article Title: A transgenic mutant mouse line accompanied by the complete deletion of interleukin-33 showed insulin and leptin resistances

doi: 10.1101/416529

Figure Lengend Snippet: The Il33 gene is completely deleted in the mutant mice and recombinant IL-33 protein restored insulin resistance in the muscle of the preobese mutant mice. ( A ) Schematic representation of the control and mutant allele surrounding the transgene integration site. Transgene integration caused the deletion of a 124.2-kb genomic DNA fragment (a blue region) at the left integration (LI) site of the mutant allele. It also caused the inversion of a 38.2-kb genomic DNA fragment with one break in the right breakpoint (RB) and the other break in the right transgene integration (RI) site (a red arrow) and the deletion of a 4.6-kb DNA fragment (a yellow region) at the right end of the mutant allele. The orientation of transcription is indicated by black arrows. White arrowheads indicate PCR primers (a1 and a3, b1-b3, and c1-c3) used for confirmation of the transgene insertion sites and breakpoint region. The orientation of the genomic DNA with respect to the centromere (cen) and telomere (tel) of chromosome 19 is indicated by black arrowheads. Flp, Flp recombinase expression vector pEF-NFLP. ( B ) PCR analysis of genomic DNA from the control and mutant mice using primers based on the inserted transgene and the flanking endogenous genomic DNA (left and center panels) or the flanking right breakpoint (right panel). Lane M contains size markers. ( C ) Real-time quantitative RT-PCR analysis in the various tissue of the control (white bars) and preobese mutant (mint green bars) mice (n = 7-10 per group). n.d., not detectable. ( D ) Insulin tolerance test (0.75 mU/g of body weight) results of the male control (white circles), the preobese mutant (mint green circles) and recombinant IL-33 (rIL-33) protein treated preobese mutant (light blue triangles) mice (n = 8-9 per group). The preobese mutant mice received an intraperitoneal injection of vehicle or rIL-33 at 1 hour before the insulin tolerance test. The control versus preobese mutant mice with vehicle: *P < 0.05, **P < 0.01; Vehicle versus rIL-33 treated preobese mutant mice: †P < 0.05, ††P < 0.01. ( E ), GIR (left), EGP (center), and R d (right) of the male control (white bars), preobese mutant (mint green bars) and rIL-33 treated preobese mutant (light blue bars) mice in the hyperinsulinemic-euglycemic clamp studies (n = 6-12 per group). *P < 0.05; **P < 0.01; n.s., not significant. ( F ) Real-time quantitative RT-PCR analysis in the muscle (left) and the liver (right) of the control (white bars) and preobese mutant (mint green bars) mice (n = 7-10 per group). n.d., not detectable. Means ± SEM.

Article Snippet: We injected 2.0 µg mouse rIL-33 (Adipogen, San Diego, California, USA) or saline as the control intraperitoneally at 1 hour before the insulin tolerance test.

Techniques: Mutagenesis, Recombinant, Expressing, Plasmid Preparation, Quantitative RT-PCR, Injection