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bs 12412r (Bioss)

Name: bs 12412r
Brand: Bioss
Rating: 94 (2 reviews)

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Bioss bs 12412r
Antibodies and assay kits

Bs 12412r, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/bs 12412r/product/Bioss
Average 94 stars, based on 2 article reviews

bs 12412r - by Bioz Stars, 2026-02

94/100 stars

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1) Product Images from "AMPK-SP1–Guided Dynein Expression Represents a New Energy-Responsive Mechanism and Therapeutic Target for Diabetic Nephropathy"

Article Title: AMPK-SP1–Guided Dynein Expression Represents a New Energy-Responsive Mechanism and Therapeutic Target for Diabetic Nephropathy

Journal: Kidney360

doi: 10.34067/KID.0000000000000392

Figure Legend Snippet: Antibodies and assay kits

Techniques Used:

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Journal: Kidney360

Article Title: AMPK-SP1–Guided Dynein Expression Represents a New Energy-Responsive Mechanism and Therapeutic Target for Diabetic Nephropathy

doi: 10.34067/KID.0000000000000392

Figure Lengend Snippet: Antibodies and assay kits

Article Snippet: Rabbit anti–phospho-SP1 (Th 453 ) , Bioss Antibodies , BS-12412R.

Techniques:

Hyperglycemia induces dynein gene expression via an AMPK/SP1-dependent mechanism. (A) Hyperglycemia-responsive dynein genes share binding motif for SP1 TF. SP1 binding motifs (red) identified in genes encoding mouse dynein subunits, using SwissRegulon tools. The promoter sequences for each individual dynein gene and their GenBank locations are highlighted in orange. ChIP primers (gray) were designed close to the SP1 binding motif and the translation starting sites (blue). (B) Workflow of crosslinking SP1 ChIP. (C) Hypothesis and research design of hyperglycemia-induced dynein gene expression via an AMPK/SP1 axis. Hyperglycemia suppresses AMPK and disinhibits SP1, which subsequently initiates the transcription of dynein subunits. (D) The fold enrichment (=2 (Ct IgG−Ct SP1) ) of dynein gene locus sequences immunoprecipitated with SP1 was quantified by ChIP-qPCR. The values were normalized to that of NG. The PCR products were confirmed by running an agarose gel. (E) SP1 activity reflected by the nuclear location of phosphorylated SP1 in podocytes with different treatments, related to the unchanged total SP1 (NG; HG; CC, an AMPK inhibitor; AICAR: an AMPK agonist). Medium containing 0.3% DMSO served as a negative control for chemical intervention. (F) Relative quantification of dynein gene transcription using Gapdh as a housekeeping gene was normalized to that of NG and was compared in a heatmap. (G) Protein levels of representative dynein subunits in podocytes with different treatments were examined using Western blot. The corresponding AMPK activity was expressed as the Thr 172 phosphorylated to total AMPK ratio (AMPK-p/AMPK). The log OD values against the β -actin housekeeping protein were normalized to that of NG. n =3, * P < 0.05 versus NG; ^ P < 0.05 SP1 siRNA versus control siRNA. AICAR, 5-aminoimidazole-4-carboxamide ribonucleoside; AMPK, AMP-activated protein kinase; CC, compound C; ChIP, chromatin immunoprecipitation; HG, high glucose; NG, normal glucose; OD, optical density; qPCR, quantitative PCR; siRNA, small interfering RNA; SP1, specificity protein 1; TF, transcription factor.

Journal: Kidney360

Article Title: AMPK-SP1–Guided Dynein Expression Represents a New Energy-Responsive Mechanism and Therapeutic Target for Diabetic Nephropathy

doi: 10.34067/KID.0000000000000392

Figure Lengend Snippet: Hyperglycemia induces dynein gene expression via an AMPK/SP1-dependent mechanism. (A) Hyperglycemia-responsive dynein genes share binding motif for SP1 TF. SP1 binding motifs (red) identified in genes encoding mouse dynein subunits, using SwissRegulon tools. The promoter sequences for each individual dynein gene and their GenBank locations are highlighted in orange. ChIP primers (gray) were designed close to the SP1 binding motif and the translation starting sites (blue). (B) Workflow of crosslinking SP1 ChIP. (C) Hypothesis and research design of hyperglycemia-induced dynein gene expression via an AMPK/SP1 axis. Hyperglycemia suppresses AMPK and disinhibits SP1, which subsequently initiates the transcription of dynein subunits. (D) The fold enrichment (=2 (Ct IgG−Ct SP1) ) of dynein gene locus sequences immunoprecipitated with SP1 was quantified by ChIP-qPCR. The values were normalized to that of NG. The PCR products were confirmed by running an agarose gel. (E) SP1 activity reflected by the nuclear location of phosphorylated SP1 in podocytes with different treatments, related to the unchanged total SP1 (NG; HG; CC, an AMPK inhibitor; AICAR: an AMPK agonist). Medium containing 0.3% DMSO served as a negative control for chemical intervention. (F) Relative quantification of dynein gene transcription using Gapdh as a housekeeping gene was normalized to that of NG and was compared in a heatmap. (G) Protein levels of representative dynein subunits in podocytes with different treatments were examined using Western blot. The corresponding AMPK activity was expressed as the Thr 172 phosphorylated to total AMPK ratio (AMPK-p/AMPK). The log OD values against the β -actin housekeeping protein were normalized to that of NG. n =3, * P < 0.05 versus NG; ^ P < 0.05 SP1 siRNA versus control siRNA. AICAR, 5-aminoimidazole-4-carboxamide ribonucleoside; AMPK, AMP-activated protein kinase; CC, compound C; ChIP, chromatin immunoprecipitation; HG, high glucose; NG, normal glucose; OD, optical density; qPCR, quantitative PCR; siRNA, small interfering RNA; SP1, specificity protein 1; TF, transcription factor.

Article Snippet: Rabbit anti–phospho-SP1 (Th 453 ) , Bioss Antibodies , BS-12412R.

Techniques: Expressing, Binding Assay, Immunoprecipitation, Agarose Gel Electrophoresis, Activity Assay, Negative Control, Western Blot, Control, Chromatin Immunoprecipitation, Real-time Polymerase Chain Reaction, Small Interfering RNA

MIT restored SP1-mediated dynein expression and dynein-mediated nephrin homeostasis in STZ-induced diabetic mice. Type 1 diabetes was induced in 8-week-old male C57BL/6J mice by single high dose injection of STZ (150 mg/kg, i.p.). Two weeks after the STZ injection, MIT diluted in NS was given via i.p. injection at the dose of 0.25 mg/kg, twice weekly for a total of eight doses. Vehicle controls received NS injections. Nondiabetic mice that received MIT injections were included in this study to exclude nephrotoxicity of MIT at this regimen. In STZ-induced diabetic mice, MIT restored SP1 activity (reflected by immunostaining of Thr 453 phosphorylated SP1 costained with podocyte nuclear marker WT1 (A) reduced nephrin protein (B) and dynein-mediated mistrafficking of nephrin (reflected by increased Dynll1 colocalizing with nephrin, C), and the upregulated expression of dynein subunits (costained with podocyte cytosol marker INF2, D). Mean fluorescence intensity of dynein subunits per podocyte was quantified for comparison. n =15 (three glomeruli or three interstitial areas per section×five mice). * P < 0.05 versus nondiabetic mice, ^ P < 0.05 versus STZ-induced diabetic mice treated with NS. Scale bar: 20 μ m. INF2, inverted formin 2; i.p., intraperitoneal; MIT, mithramycin; NS, normal saline; STZ, streptozotocin.

Journal: Kidney360

Article Title: AMPK-SP1–Guided Dynein Expression Represents a New Energy-Responsive Mechanism and Therapeutic Target for Diabetic Nephropathy

doi: 10.34067/KID.0000000000000392

Figure Lengend Snippet: MIT restored SP1-mediated dynein expression and dynein-mediated nephrin homeostasis in STZ-induced diabetic mice. Type 1 diabetes was induced in 8-week-old male C57BL/6J mice by single high dose injection of STZ (150 mg/kg, i.p.). Two weeks after the STZ injection, MIT diluted in NS was given via i.p. injection at the dose of 0.25 mg/kg, twice weekly for a total of eight doses. Vehicle controls received NS injections. Nondiabetic mice that received MIT injections were included in this study to exclude nephrotoxicity of MIT at this regimen. In STZ-induced diabetic mice, MIT restored SP1 activity (reflected by immunostaining of Thr 453 phosphorylated SP1 costained with podocyte nuclear marker WT1 (A) reduced nephrin protein (B) and dynein-mediated mistrafficking of nephrin (reflected by increased Dynll1 colocalizing with nephrin, C), and the upregulated expression of dynein subunits (costained with podocyte cytosol marker INF2, D). Mean fluorescence intensity of dynein subunits per podocyte was quantified for comparison. n =15 (three glomeruli or three interstitial areas per section×five mice). * P < 0.05 versus nondiabetic mice, ^ P < 0.05 versus STZ-induced diabetic mice treated with NS. Scale bar: 20 μ m. INF2, inverted formin 2; i.p., intraperitoneal; MIT, mithramycin; NS, normal saline; STZ, streptozotocin.

Article Snippet: Rabbit anti–phospho-SP1 (Th 453 ) , Bioss Antibodies , BS-12412R.

Techniques: Expressing, Injection, Activity Assay, Immunostaining, Marker, Fluorescence, Comparison, Saline

$HG impaired nephrin proteosis via AMPK/SP1-regulated dynein expression. (A) Coimmunostaining of nephrin and Dynll1 in podocytes cultured under different conditions: NG (NG+0.3% DMSO); HG (HG+0.3% DMSO); HG in the presence of MIT (0.1 μ M MIT); or AICAR (0.5 mM). (B–D) Nephrin expressed on podocyte surface underwent crosslink-induced endocytosis induced by fluorophore-labeled antinephrin. The postendocytic trafficking of nephrin in HG-cultured podocytes in the presence of MIT or Ciliobrevin D (50 µ M) versus control cells (HG+DMSO) was visualized using live cell imaging and analyzed using the TrackMate and KymographClear plugins of Fiji/ImageJ software. With TrackMate (B), faster retrograde trafficking of nephrin (from surface membrane to cytosol) is displayed in warmer colors, and slower tracks are displayed in cooler colors. In the Kymograph (C), the retrograde, static, and anterograde (from cytosol to surface membrane) tracking events are displayed in red, blue, and green. (D) The fraction and velocities of the trafficking events were quantified using KymographDirect software. * P < 0.05 versus HG+DMSO.$

Journal: Kidney360

Article Title: AMPK-SP1–Guided Dynein Expression Represents a New Energy-Responsive Mechanism and Therapeutic Target for Diabetic Nephropathy

doi: 10.34067/KID.0000000000000392

Figure Lengend Snippet: HG impaired nephrin proteosis via AMPK/SP1-regulated dynein expression. (A) Coimmunostaining of nephrin and Dynll1 in podocytes cultured under different conditions: NG (NG+0.3% DMSO); HG (HG+0.3% DMSO); HG in the presence of MIT (0.1 μ M MIT); or AICAR (0.5 mM). (B–D) Nephrin expressed on podocyte surface underwent crosslink-induced endocytosis induced by fluorophore-labeled antinephrin. The postendocytic trafficking of nephrin in HG-cultured podocytes in the presence of MIT or Ciliobrevin D (50 µ M) versus control cells (HG+DMSO) was visualized using live cell imaging and analyzed using the TrackMate and KymographClear plugins of Fiji/ImageJ software. With TrackMate (B), faster retrograde trafficking of nephrin (from surface membrane to cytosol) is displayed in warmer colors, and slower tracks are displayed in cooler colors. In the Kymograph (C), the retrograde, static, and anterograde (from cytosol to surface membrane) tracking events are displayed in red, blue, and green. (D) The fraction and velocities of the trafficking events were quantified using KymographDirect software. * P < 0.05 versus HG+DMSO.

Article Snippet: Rabbit anti–phospho-SP1 (Th 453 ) , Bioss Antibodies , BS-12412R.

Techniques: Expressing, Cell Culture, Labeling, Control, Live Cell Imaging, Software, Membrane

Journal: Kidney360

Article Title: AMPK-SP1–Guided Dynein Expression Represents a New Energy-Responsive Mechanism and Therapeutic Target for Diabetic Nephropathy

doi: 10.34067/KID.0000000000000392

Figure Lengend Snippet: Small interfering RNA duplex sequences

Article Snippet: Rabbit anti–phospho-SP1 (Th 453 ) , Bioss Antibodies , BS-12412R.

Techniques: Small Interfering RNA, Control

Journal: Kidney360

Article Title: AMPK-SP1–Guided Dynein Expression Represents a New Energy-Responsive Mechanism and Therapeutic Target for Diabetic Nephropathy

doi: 10.34067/KID.0000000000000392

Figure Lengend Snippet: Antibodies and assay kits

Article Snippet: Rabbit anti–phospho-SP1 (Th 453 ) , Bioss Antibodies , BS-12412R.

Techniques:

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1) Product Images from "AMPK-SP1–Guided Dynein Expression Represents a New Energy-Responsive Mechanism and Therapeutic Target for Diabetic Nephropathy"

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