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Proteintech 11βhsd1
11βhsd1, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/hsd11b1/pm41650548-85-29-30?v=Proteintech
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11βhsd1 - by Bioz Stars, 2026-07
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FKBP51 promotes increased <t>HSD11B1</t> expression, with baseline HSD11B1 levels elevated in leiomyomatous uteri. HSD11B1 levels in leiomyoma cells (n = 4) (A) by RNA-sequencing representing fragments per kilobase of transcript per million mapped reads (FPKM) and (B) by qPCR. Dexamethasone (DEX) treatment increased HSD11B1 mRNA levels in control siRNA-transfected cells vs vehicle treatment (Cont). However, this DEX-induced upregulation was blunted in FKBP5- silenced cells. (C) In situ HSD11B1 mRNA levels are increased in paired leiomyoma tissue samples (n = 17 paired, n = 17 leiomyoma) relative to normal myometrium samples (n = 16). (D) HSD11β1 immunostaining (brown) in normal myometrium (n = 6), paired (n = 6) and leiomyoma (n = 6) tissue samples, with decreased expression seen in normal tissues as quantified by H score. Inset represents negative control in each tissue sample. Bars represent mean ± standard error of the mean. * P < .05, # P < .001, ** P = .002, ## P = .01 , $ P = .04. RNA sequencing raw data available in the NCBI GEO repository, accession number GSE292403 .
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FKBP51 promotes increased <t>HSD11B1</t> expression, with baseline HSD11B1 levels elevated in leiomyomatous uteri. HSD11B1 levels in leiomyoma cells (n = 4) (A) by RNA-sequencing representing fragments per kilobase of transcript per million mapped reads (FPKM) and (B) by qPCR. Dexamethasone (DEX) treatment increased HSD11B1 mRNA levels in control siRNA-transfected cells vs vehicle treatment (Cont). However, this DEX-induced upregulation was blunted in FKBP5- silenced cells. (C) In situ HSD11B1 mRNA levels are increased in paired leiomyoma tissue samples (n = 17 paired, n = 17 leiomyoma) relative to normal myometrium samples (n = 16). (D) HSD11β1 immunostaining (brown) in normal myometrium (n = 6), paired (n = 6) and leiomyoma (n = 6) tissue samples, with decreased expression seen in normal tissues as quantified by H score. Inset represents negative control in each tissue sample. Bars represent mean ± standard error of the mean. * P < .05, # P < .001, ** P = .002, ## P = .01 , $ P = .04. RNA sequencing raw data available in the NCBI GEO repository, accession number GSE292403 .
11βhsd1, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/hsd11b1/pm41650548-85-29-30?v=Proteintech
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FKBP51 promotes increased <t>HSD11B1</t> expression, with baseline HSD11B1 levels elevated in leiomyomatous uteri. HSD11B1 levels in leiomyoma cells (n = 4) (A) by RNA-sequencing representing fragments per kilobase of transcript per million mapped reads (FPKM) and (B) by qPCR. Dexamethasone (DEX) treatment increased HSD11B1 mRNA levels in control siRNA-transfected cells vs vehicle treatment (Cont). However, this DEX-induced upregulation was blunted in FKBP5- silenced cells. (C) In situ HSD11B1 mRNA levels are increased in paired leiomyoma tissue samples (n = 17 paired, n = 17 leiomyoma) relative to normal myometrium samples (n = 16). (D) HSD11β1 immunostaining (brown) in normal myometrium (n = 6), paired (n = 6) and leiomyoma (n = 6) tissue samples, with decreased expression seen in normal tissues as quantified by H score. Inset represents negative control in each tissue sample. Bars represent mean ± standard error of the mean. * P < .05, # P < .001, ** P = .002, ## P = .01 , $ P = .04. RNA sequencing raw data available in the NCBI GEO repository, accession number GSE292403 .
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FKBP51 promotes increased HSD11B1 expression, with baseline HSD11B1 levels elevated in leiomyomatous uteri. HSD11B1 levels in leiomyoma cells (n = 4) (A) by RNA-sequencing representing fragments per kilobase of transcript per million mapped reads (FPKM) and (B) by qPCR. Dexamethasone (DEX) treatment increased HSD11B1 mRNA levels in control siRNA-transfected cells vs vehicle treatment (Cont). However, this DEX-induced upregulation was blunted in FKBP5- silenced cells. (C) In situ HSD11B1 mRNA levels are increased in paired leiomyoma tissue samples (n = 17 paired, n = 17 leiomyoma) relative to normal myometrium samples (n = 16). (D) <t>HSD11β1</t> immunostaining (brown) in normal myometrium (n = 6), paired (n = 6) and leiomyoma (n = 6) tissue samples, with decreased expression seen in normal tissues as quantified by H score. Inset represents negative control in each tissue sample. Bars represent mean ± standard error of the mean. * P < .05, # P < .001, ** P = .002, ## P = .01 , $ P = .04. RNA sequencing raw data available in the NCBI GEO repository, accession number GSE292403 .
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Thermo Fisher gene exp hsd11b1 cf02626817 m1
Relative gene expression of PGR ( A ), GR / NR3C1 ( B ), <t>HSD11B1</t> ( C ), HSD11B2 ( D ), PTGS2 / COX2 ( E ), PTGES ( F ), PGFS / AKR1C3 ( G ), PGT ( H ) and HPGD ( I ) in the placenta of bitches at prepartum luteolysis and presenting with primary uterine inertia (PUI). The relative gene expression was determined using semi-quantitative real-time TaqMan PCR, and the results are expressed as geometric means ± geometric standard deviation. Student’s t test was used to compare the detected mRNA availability between luteolysis and PUI groups. Bars with asterisks differ at: * p < 0.05, ** p < 0.01, *** p < 0.001.
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(A) Bar chart displaying the top 10 upregulated and downregulated transcription factor activity scores in the MgIG (ALD+MgIG) group compared to the A-Ctrl (ALD only) group. (B) The glide score of MgIG binding to the protein structure as determined by molecular docking analysis. (C, D) RMSD and RMSF analysis of the three systems: <t>APO-HSD11B1</t> (blue) represents unbound HSD11B1 in a physiological saline system, Compound-HSD11B1 (red) represents HSD11B1 bound to MgIG in a physiological saline system, and EtOH-HSD11B1 (green) represents HSD11B1 bound to MgIG in a 0.1 mg/mL ethanol solvent system. (E, F) Molecular modeling analysis of MgIG binding at the HSD11B1 domain in normal saline and ethanol systems. Left: Cartoon view of MgIG at the HSD11B1 binding site. Right: Close-up surface view of MgIG at the HSD11B1 binding sites. (G) Hydrogen bond analysis of HSD11B1-MgIG interactions in normal saline and ethanol systems. (H, I) The microscale thermophoresis (MST) assay demonstrated direct binding between varying doses of MgIG and human HSD11B1 protein at residues 187. WT: wild-type HSD11B1; M1, M2, M3: point mutations at Tyr177, Tyr183, and Lys187, respectively.
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The effect of RELA, MIRI, and EPL on mRNA expression of MR/GR activity regulators. The mRNA levels of glucocorticoid-activating and -inactivating enzymes were monitored in skin from mice treated as in . ( A ) <t>Hsd11b1</t> mRNA expression was not significantly altered by RELA, MIRI, or EPL treatment. ( B ) Hsd11b2 mRNA expression was not significantly altered by RELA, MIRI, or EPL treatment. n = 7–8.
Gene Exp Hsd11b1 Mm00476182 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech anti hsd11b1
The effect of RELA, MIRI, and EPL on mRNA expression of MR/GR activity regulators. The mRNA levels of glucocorticoid-activating and -inactivating enzymes were monitored in skin from mice treated as in . ( A ) <t>Hsd11b1</t> mRNA expression was not significantly altered by RELA, MIRI, or EPL treatment. ( B ) Hsd11b2 mRNA expression was not significantly altered by RELA, MIRI, or EPL treatment. n = 7–8.
Anti Hsd11b1, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech anti 11β hsd1
The effect of RELA, MIRI, and EPL on mRNA expression of MR/GR activity regulators. The mRNA levels of glucocorticoid-activating and -inactivating enzymes were monitored in skin from mice treated as in . ( A ) <t>Hsd11b1</t> mRNA expression was not significantly altered by RELA, MIRI, or EPL treatment. ( B ) Hsd11b2 mRNA expression was not significantly altered by RELA, MIRI, or EPL treatment. n = 7–8.
Anti 11β Hsd1, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


FKBP51 promotes increased HSD11B1 expression, with baseline HSD11B1 levels elevated in leiomyomatous uteri. HSD11B1 levels in leiomyoma cells (n = 4) (A) by RNA-sequencing representing fragments per kilobase of transcript per million mapped reads (FPKM) and (B) by qPCR. Dexamethasone (DEX) treatment increased HSD11B1 mRNA levels in control siRNA-transfected cells vs vehicle treatment (Cont). However, this DEX-induced upregulation was blunted in FKBP5- silenced cells. (C) In situ HSD11B1 mRNA levels are increased in paired leiomyoma tissue samples (n = 17 paired, n = 17 leiomyoma) relative to normal myometrium samples (n = 16). (D) HSD11β1 immunostaining (brown) in normal myometrium (n = 6), paired (n = 6) and leiomyoma (n = 6) tissue samples, with decreased expression seen in normal tissues as quantified by H score. Inset represents negative control in each tissue sample. Bars represent mean ± standard error of the mean. * P < .05, # P < .001, ** P = .002, ## P = .01 , $ P = .04. RNA sequencing raw data available in the NCBI GEO repository, accession number GSE292403 .

Journal: The Journal of Clinical Endocrinology and Metabolism

Article Title: Increased HSD11β1 Expression in Human Leiomyomatous Uteri: Implication for Enhanced Glucocorticoid Signaling

doi: 10.1210/clinem/dgaf255

Figure Lengend Snippet: FKBP51 promotes increased HSD11B1 expression, with baseline HSD11B1 levels elevated in leiomyomatous uteri. HSD11B1 levels in leiomyoma cells (n = 4) (A) by RNA-sequencing representing fragments per kilobase of transcript per million mapped reads (FPKM) and (B) by qPCR. Dexamethasone (DEX) treatment increased HSD11B1 mRNA levels in control siRNA-transfected cells vs vehicle treatment (Cont). However, this DEX-induced upregulation was blunted in FKBP5- silenced cells. (C) In situ HSD11B1 mRNA levels are increased in paired leiomyoma tissue samples (n = 17 paired, n = 17 leiomyoma) relative to normal myometrium samples (n = 16). (D) HSD11β1 immunostaining (brown) in normal myometrium (n = 6), paired (n = 6) and leiomyoma (n = 6) tissue samples, with decreased expression seen in normal tissues as quantified by H score. Inset represents negative control in each tissue sample. Bars represent mean ± standard error of the mean. * P < .05, # P < .001, ** P = .002, ## P = .01 , $ P = .04. RNA sequencing raw data available in the NCBI GEO repository, accession number GSE292403 .

Article Snippet: The full name and Taq-Man Probe Assay IDs for each target gene include: FK506-binding protein 5 ( FKBP5 )- Hs01561006_m1; Hydroxysteroid 11-β dehydrogenase 1 ( HSD11B1) - Hs01547870_m1; IL-1 receptor type 1 ( IL1R1 )- Hs00991002_m1; TSC22 domain family member 3 ( TSC22D3 )- Hs00608272_m1; alcohol dehydrogenase 1B, β polypeptide ( ADH1B )- Hs00605175_m1; Gremlin 1, DAN family BMP antagonist ( GREM1 )- Hs00171951_m1; IGF-binding protein 5 ( IGFBP5 )- Hs00181213_m1; adhesion molecule with Ig-like domain 2 ( AMIGO2 )- Hs05001325_s1; laminin subunit alpha 2 ( LAMA2 )- Hs00166308_m1; fibronectin 1 ( FN1 )- Hs00365052_m1; calponin 1 ( CNN1 )- Hs00959434_m1; actin β ( ACTB )- Hs99999903_m1; and glyceraldehyde-3-phosphate dehydrogenase ( GAPDH )- Hs99999905_m1.

Techniques: Expressing, RNA Sequencing, Control, Transfection, In Situ, Immunostaining, Negative Control

Dexamethasone (DEX) treatment increases HSD11B1 expression in normal myometrial and human endometrial stromal cell cultures but to a lesser extent than in leiomyoma cells, in a FKBP51-dependent manner. (A) FKBP5 knockdown efficiency in normal myometrial cell (TM; n = 4) and human endometrial stromal cell (HESC; n = 4) cultures was confirmed by qPCR, with significantly decreased FKBP5 mRNA levels seen in FKBP5 siRNA-transfected cells (FkSi) vs control siRNA-transfected cells (Cont). DEX treatment increased FKBP5 mRNA levels in TM and HESC cell lines. This DEX-induced increase in FKBP5 levels was less pronounced in FKBP5 -silenced cells (FkSi + DEX) for both cell lines. (B) DEX treatment increased HSD11B1 mRNA levels in control siRNA-transfected TM (n = 4), HESC (n = 4), and leiomyoma (TLM; n = 4) cells (DEX) vs vehicle treatment (Cont). This increase was blunted following FKBP5 knockdown (FkSi + DEX vs FkSi; fold change relative to Cont). Bars represent mean ± standard error of the mean. * P < .05.

Journal: The Journal of Clinical Endocrinology and Metabolism

Article Title: Increased HSD11β1 Expression in Human Leiomyomatous Uteri: Implication for Enhanced Glucocorticoid Signaling

doi: 10.1210/clinem/dgaf255

Figure Lengend Snippet: Dexamethasone (DEX) treatment increases HSD11B1 expression in normal myometrial and human endometrial stromal cell cultures but to a lesser extent than in leiomyoma cells, in a FKBP51-dependent manner. (A) FKBP5 knockdown efficiency in normal myometrial cell (TM; n = 4) and human endometrial stromal cell (HESC; n = 4) cultures was confirmed by qPCR, with significantly decreased FKBP5 mRNA levels seen in FKBP5 siRNA-transfected cells (FkSi) vs control siRNA-transfected cells (Cont). DEX treatment increased FKBP5 mRNA levels in TM and HESC cell lines. This DEX-induced increase in FKBP5 levels was less pronounced in FKBP5 -silenced cells (FkSi + DEX) for both cell lines. (B) DEX treatment increased HSD11B1 mRNA levels in control siRNA-transfected TM (n = 4), HESC (n = 4), and leiomyoma (TLM; n = 4) cells (DEX) vs vehicle treatment (Cont). This increase was blunted following FKBP5 knockdown (FkSi + DEX vs FkSi; fold change relative to Cont). Bars represent mean ± standard error of the mean. * P < .05.

Article Snippet: The full name and Taq-Man Probe Assay IDs for each target gene include: FK506-binding protein 5 ( FKBP5 )- Hs01561006_m1; Hydroxysteroid 11-β dehydrogenase 1 ( HSD11B1) - Hs01547870_m1; IL-1 receptor type 1 ( IL1R1 )- Hs00991002_m1; TSC22 domain family member 3 ( TSC22D3 )- Hs00608272_m1; alcohol dehydrogenase 1B, β polypeptide ( ADH1B )- Hs00605175_m1; Gremlin 1, DAN family BMP antagonist ( GREM1 )- Hs00171951_m1; IGF-binding protein 5 ( IGFBP5 )- Hs00181213_m1; adhesion molecule with Ig-like domain 2 ( AMIGO2 )- Hs05001325_s1; laminin subunit alpha 2 ( LAMA2 )- Hs00166308_m1; fibronectin 1 ( FN1 )- Hs00365052_m1; calponin 1 ( CNN1 )- Hs00959434_m1; actin β ( ACTB )- Hs99999903_m1; and glyceraldehyde-3-phosphate dehydrogenase ( GAPDH )- Hs99999905_m1.

Techniques: Expressing, Knockdown, Transfection, Control

FKBP51 promotes increased HSD11B1 expression, with baseline HSD11B1 levels elevated in leiomyomatous uteri. HSD11B1 levels in leiomyoma cells (n = 4) (A) by RNA-sequencing representing fragments per kilobase of transcript per million mapped reads (FPKM) and (B) by qPCR. Dexamethasone (DEX) treatment increased HSD11B1 mRNA levels in control siRNA-transfected cells vs vehicle treatment (Cont). However, this DEX-induced upregulation was blunted in FKBP5- silenced cells. (C) In situ HSD11B1 mRNA levels are increased in paired leiomyoma tissue samples (n = 17 paired, n = 17 leiomyoma) relative to normal myometrium samples (n = 16). (D) HSD11β1 immunostaining (brown) in normal myometrium (n = 6), paired (n = 6) and leiomyoma (n = 6) tissue samples, with decreased expression seen in normal tissues as quantified by H score. Inset represents negative control in each tissue sample. Bars represent mean ± standard error of the mean. * P < .05, # P < .001, ** P = .002, ## P = .01 , $ P = .04. RNA sequencing raw data available in the NCBI GEO repository, accession number GSE292403 .

Journal: The Journal of Clinical Endocrinology and Metabolism

Article Title: Increased HSD11β1 Expression in Human Leiomyomatous Uteri: Implication for Enhanced Glucocorticoid Signaling

doi: 10.1210/clinem/dgaf255

Figure Lengend Snippet: FKBP51 promotes increased HSD11B1 expression, with baseline HSD11B1 levels elevated in leiomyomatous uteri. HSD11B1 levels in leiomyoma cells (n = 4) (A) by RNA-sequencing representing fragments per kilobase of transcript per million mapped reads (FPKM) and (B) by qPCR. Dexamethasone (DEX) treatment increased HSD11B1 mRNA levels in control siRNA-transfected cells vs vehicle treatment (Cont). However, this DEX-induced upregulation was blunted in FKBP5- silenced cells. (C) In situ HSD11B1 mRNA levels are increased in paired leiomyoma tissue samples (n = 17 paired, n = 17 leiomyoma) relative to normal myometrium samples (n = 16). (D) HSD11β1 immunostaining (brown) in normal myometrium (n = 6), paired (n = 6) and leiomyoma (n = 6) tissue samples, with decreased expression seen in normal tissues as quantified by H score. Inset represents negative control in each tissue sample. Bars represent mean ± standard error of the mean. * P < .05, # P < .001, ** P = .002, ## P = .01 , $ P = .04. RNA sequencing raw data available in the NCBI GEO repository, accession number GSE292403 .

Article Snippet: After washing in Tris-buffered saline (TBS), slides were incubated with 5% normal goat serum (Vector Labs, Burlingame, CA) for 30 minutes at room temperature, then incubated overnight at 4 °C in rabbit polyclonal antibody against HSD11β1 (1:100, Atlas Antibodies Cat# HPA047729, RRID:AB_2680135) in 2.5% goat serum.

Techniques: Expressing, RNA Sequencing, Control, Transfection, In Situ, Immunostaining, Negative Control

Schematic illustration of the potential mechanism by which enhanced FKBP51-GR signaling contributes to the pathogenesis of leiomyoma. Elevated levels of FKBP51 augment glucocorticoid-induced GR-mediated upregulation of HSD11β1, which converts inactive cortisone to active cortisol, leading to sustained intracellular glucocorticoid signaling in leiomyoma cells. This FKBP51-GR-HSD11β1 relationship generates an intracellular pathological circle, leading to increased expression of extracellular matrix (ECM) genes and decreased levels of genes expressed by smooth muscle cells, supporting a switch from a smooth muscle to myofibroblast phenotype, thereby contributing to the pathogenesis of leiomyoma.

Journal: The Journal of Clinical Endocrinology and Metabolism

Article Title: Increased HSD11β1 Expression in Human Leiomyomatous Uteri: Implication for Enhanced Glucocorticoid Signaling

doi: 10.1210/clinem/dgaf255

Figure Lengend Snippet: Schematic illustration of the potential mechanism by which enhanced FKBP51-GR signaling contributes to the pathogenesis of leiomyoma. Elevated levels of FKBP51 augment glucocorticoid-induced GR-mediated upregulation of HSD11β1, which converts inactive cortisone to active cortisol, leading to sustained intracellular glucocorticoid signaling in leiomyoma cells. This FKBP51-GR-HSD11β1 relationship generates an intracellular pathological circle, leading to increased expression of extracellular matrix (ECM) genes and decreased levels of genes expressed by smooth muscle cells, supporting a switch from a smooth muscle to myofibroblast phenotype, thereby contributing to the pathogenesis of leiomyoma.

Article Snippet: After washing in Tris-buffered saline (TBS), slides were incubated with 5% normal goat serum (Vector Labs, Burlingame, CA) for 30 minutes at room temperature, then incubated overnight at 4 °C in rabbit polyclonal antibody against HSD11β1 (1:100, Atlas Antibodies Cat# HPA047729, RRID:AB_2680135) in 2.5% goat serum.

Techniques: Expressing

Relative gene expression of PGR ( A ), GR / NR3C1 ( B ), HSD11B1 ( C ), HSD11B2 ( D ), PTGS2 / COX2 ( E ), PTGES ( F ), PGFS / AKR1C3 ( G ), PGT ( H ) and HPGD ( I ) in the placenta of bitches at prepartum luteolysis and presenting with primary uterine inertia (PUI). The relative gene expression was determined using semi-quantitative real-time TaqMan PCR, and the results are expressed as geometric means ± geometric standard deviation. Student’s t test was used to compare the detected mRNA availability between luteolysis and PUI groups. Bars with asterisks differ at: * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Animals : an Open Access Journal from MDPI

Article Title: Primary Uterine Inertia (PUI) in Dogs Is Associated with Impaired Placental Availability of Factors Involved in the Parturition Cascade

doi: 10.3390/ani15203043

Figure Lengend Snippet: Relative gene expression of PGR ( A ), GR / NR3C1 ( B ), HSD11B1 ( C ), HSD11B2 ( D ), PTGS2 / COX2 ( E ), PTGES ( F ), PGFS / AKR1C3 ( G ), PGT ( H ) and HPGD ( I ) in the placenta of bitches at prepartum luteolysis and presenting with primary uterine inertia (PUI). The relative gene expression was determined using semi-quantitative real-time TaqMan PCR, and the results are expressed as geometric means ± geometric standard deviation. Student’s t test was used to compare the detected mRNA availability between luteolysis and PUI groups. Bars with asterisks differ at: * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: HSD11B1 , Hydroxysteroid 11β dehydrogenase 1 , , Prod. No. Cf02626817_m1 , , 67.

Techniques: Gene Expression, Standard Deviation

(A) Bar chart displaying the top 10 upregulated and downregulated transcription factor activity scores in the MgIG (ALD+MgIG) group compared to the A-Ctrl (ALD only) group. (B) The glide score of MgIG binding to the protein structure as determined by molecular docking analysis. (C, D) RMSD and RMSF analysis of the three systems: APO-HSD11B1 (blue) represents unbound HSD11B1 in a physiological saline system, Compound-HSD11B1 (red) represents HSD11B1 bound to MgIG in a physiological saline system, and EtOH-HSD11B1 (green) represents HSD11B1 bound to MgIG in a 0.1 mg/mL ethanol solvent system. (E, F) Molecular modeling analysis of MgIG binding at the HSD11B1 domain in normal saline and ethanol systems. Left: Cartoon view of MgIG at the HSD11B1 binding site. Right: Close-up surface view of MgIG at the HSD11B1 binding sites. (G) Hydrogen bond analysis of HSD11B1-MgIG interactions in normal saline and ethanol systems. (H, I) The microscale thermophoresis (MST) assay demonstrated direct binding between varying doses of MgIG and human HSD11B1 protein at residues 187. WT: wild-type HSD11B1; M1, M2, M3: point mutations at Tyr177, Tyr183, and Lys187, respectively.

Journal: bioRxiv

Article Title: Magnesium isoglycyrrhizinate alleviates alcohol-associated liver disease through targeting HSD11B1

doi: 10.1101/2025.10.02.679991

Figure Lengend Snippet: (A) Bar chart displaying the top 10 upregulated and downregulated transcription factor activity scores in the MgIG (ALD+MgIG) group compared to the A-Ctrl (ALD only) group. (B) The glide score of MgIG binding to the protein structure as determined by molecular docking analysis. (C, D) RMSD and RMSF analysis of the three systems: APO-HSD11B1 (blue) represents unbound HSD11B1 in a physiological saline system, Compound-HSD11B1 (red) represents HSD11B1 bound to MgIG in a physiological saline system, and EtOH-HSD11B1 (green) represents HSD11B1 bound to MgIG in a 0.1 mg/mL ethanol solvent system. (E, F) Molecular modeling analysis of MgIG binding at the HSD11B1 domain in normal saline and ethanol systems. Left: Cartoon view of MgIG at the HSD11B1 binding site. Right: Close-up surface view of MgIG at the HSD11B1 binding sites. (G) Hydrogen bond analysis of HSD11B1-MgIG interactions in normal saline and ethanol systems. (H, I) The microscale thermophoresis (MST) assay demonstrated direct binding between varying doses of MgIG and human HSD11B1 protein at residues 187. WT: wild-type HSD11B1; M1, M2, M3: point mutations at Tyr177, Tyr183, and Lys187, respectively.

Article Snippet: An antibody against HSD11B1 (#AF3397) was purchased from R&D Systems (Minneapolis, MN, USA).

Techniques: Activity Assay, Binding Assay, Saline, Solvent, Microscale Thermophoresis

(A) Quantitative PCR validation of RNA-seq results revealed changes in Hsd11b1 gene expression in AML-12 cells treated with ethanol/PA, with or without 0.25 mg/ml MgIG co-treatment (n = 4). (B, C) Quantitative PCR confirmed the knockdown efficiency of Hsd11b1 (siRNA) and the overexpression efficiency of Idi1 (plasmid) in AML-12 cells, and cell viability changes were assessed 48 h after transfection (n = 4). (D) Nile Red staining area (%) with corresponding representative cell staining images (n=4). (E, F) Western blot results for TNF-α, IL-6, Bax, and Bcl-2 and cell supernatant results for TNF-α and IL-6 in AML-12 cells treated with ethanol/PA and ethanol/PA + MgIG, with or without Hsd11b1 knockdown/overexpression (n = 3). Data are expressed as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001. Scale bar: 20 μm.

Journal: bioRxiv

Article Title: Magnesium isoglycyrrhizinate alleviates alcohol-associated liver disease through targeting HSD11B1

doi: 10.1101/2025.10.02.679991

Figure Lengend Snippet: (A) Quantitative PCR validation of RNA-seq results revealed changes in Hsd11b1 gene expression in AML-12 cells treated with ethanol/PA, with or without 0.25 mg/ml MgIG co-treatment (n = 4). (B, C) Quantitative PCR confirmed the knockdown efficiency of Hsd11b1 (siRNA) and the overexpression efficiency of Idi1 (plasmid) in AML-12 cells, and cell viability changes were assessed 48 h after transfection (n = 4). (D) Nile Red staining area (%) with corresponding representative cell staining images (n=4). (E, F) Western blot results for TNF-α, IL-6, Bax, and Bcl-2 and cell supernatant results for TNF-α and IL-6 in AML-12 cells treated with ethanol/PA and ethanol/PA + MgIG, with or without Hsd11b1 knockdown/overexpression (n = 3). Data are expressed as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001. Scale bar: 20 μm.

Article Snippet: An antibody against HSD11B1 (#AF3397) was purchased from R&D Systems (Minneapolis, MN, USA).

Techniques: Real-time Polymerase Chain Reaction, Biomarker Discovery, RNA Sequencing, Gene Expression, Knockdown, Over Expression, Plasmid Preparation, Transfection, Staining, Western Blot

(A, B) Co-IP was used to verify the direct binding between HSD11B1 and SREBP2 with or without MgIG treatment. (C, D) Alterations in protein levels of HSD11B1, p-SREBP2, n-SREBP2, and IDI1 in AML-12 cells induced by EtOH/PA, following knockdown or overexpression of Hsd11b1 , with and without MgIG treatment (n = 3). (E) Immunofluorescent staining was conducted to visualize the distribution and expression of SREBP2 (red) in EtoH/PA-induced AML-12 cells, with or without MgIG, following Hsd11b1 knockdown or overexpression. (F) Co-IP was used to verify the direct binding between HSD11B1 and IDI1. (G) Effects of Srebp2 on Idi1 transcriptional regulation were measured by luciferase assays in AML-12 and 293T cell lines. Idi1-wild-type (WT) or Idi1-mutant (Mut), plasmids with WT promoter cDNA clone of Idi1 or with mutant promoter cDNA clone plasmid; pRL-TK, an internal control reporter plasmid. (H, I) The expression levels of Hsd11b1 , Srebp2 , and Idi1 in normal liver were measured following the knockdown of Hsd11b1 , Srebp2 , and Idi1 , or the overexpression of Hsd11b1 and Idi1 , respectively (n = 4). (J, K) The expression levels of Hsd11b1 , Srebp2 , and Idi1 in ALD liver were measured following the knockdown of Hsd11b1 , Srebp2 , and Idi1 , or the overexpression of Hsd11b1 and Idi1 , respectively (n = 5). Data are expressed as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001. **** P < 0.0001. Scale bar: 10 μm.

Journal: bioRxiv

Article Title: Magnesium isoglycyrrhizinate alleviates alcohol-associated liver disease through targeting HSD11B1

doi: 10.1101/2025.10.02.679991

Figure Lengend Snippet: (A, B) Co-IP was used to verify the direct binding between HSD11B1 and SREBP2 with or without MgIG treatment. (C, D) Alterations in protein levels of HSD11B1, p-SREBP2, n-SREBP2, and IDI1 in AML-12 cells induced by EtOH/PA, following knockdown or overexpression of Hsd11b1 , with and without MgIG treatment (n = 3). (E) Immunofluorescent staining was conducted to visualize the distribution and expression of SREBP2 (red) in EtoH/PA-induced AML-12 cells, with or without MgIG, following Hsd11b1 knockdown or overexpression. (F) Co-IP was used to verify the direct binding between HSD11B1 and IDI1. (G) Effects of Srebp2 on Idi1 transcriptional regulation were measured by luciferase assays in AML-12 and 293T cell lines. Idi1-wild-type (WT) or Idi1-mutant (Mut), plasmids with WT promoter cDNA clone of Idi1 or with mutant promoter cDNA clone plasmid; pRL-TK, an internal control reporter plasmid. (H, I) The expression levels of Hsd11b1 , Srebp2 , and Idi1 in normal liver were measured following the knockdown of Hsd11b1 , Srebp2 , and Idi1 , or the overexpression of Hsd11b1 and Idi1 , respectively (n = 4). (J, K) The expression levels of Hsd11b1 , Srebp2 , and Idi1 in ALD liver were measured following the knockdown of Hsd11b1 , Srebp2 , and Idi1 , or the overexpression of Hsd11b1 and Idi1 , respectively (n = 5). Data are expressed as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001. **** P < 0.0001. Scale bar: 10 μm.

Article Snippet: An antibody against HSD11B1 (#AF3397) was purchased from R&D Systems (Minneapolis, MN, USA).

Techniques: Co-Immunoprecipitation Assay, Binding Assay, Knockdown, Over Expression, Staining, Expressing, Luciferase, Mutagenesis, Plasmid Preparation, Control

(A-D) Representative liver H&E and Oil Red O staining results from ALD mice with Hsd11b1 , Srebp2 , or Idi1 knockdown or overexpression, with and/or without MgIG co-treatment. Changes in quantitative NAS (NAFLD activity score) and Oil Red staining (area %) were calculated and analyzed (n = 5). (E-F) Changes of serum ALT and TNF-α from ALD mice with Hsd11b1 , Srebp2 , or Idi1 knockdown or overexpression, with and/or without MgIG co-treatment (n = 5). (G) Alterations in protein levels of HSD11B1, p-SREBP2, n-SREBP 2, and Idi1 in ALD mice, following knockdown or overexpression of Hsd11b1 , with and without MgIG co-treatment (n = 3). Data are expressed as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Scale bar: 50 μm.

Journal: bioRxiv

Article Title: Magnesium isoglycyrrhizinate alleviates alcohol-associated liver disease through targeting HSD11B1

doi: 10.1101/2025.10.02.679991

Figure Lengend Snippet: (A-D) Representative liver H&E and Oil Red O staining results from ALD mice with Hsd11b1 , Srebp2 , or Idi1 knockdown or overexpression, with and/or without MgIG co-treatment. Changes in quantitative NAS (NAFLD activity score) and Oil Red staining (area %) were calculated and analyzed (n = 5). (E-F) Changes of serum ALT and TNF-α from ALD mice with Hsd11b1 , Srebp2 , or Idi1 knockdown or overexpression, with and/or without MgIG co-treatment (n = 5). (G) Alterations in protein levels of HSD11B1, p-SREBP2, n-SREBP 2, and Idi1 in ALD mice, following knockdown or overexpression of Hsd11b1 , with and without MgIG co-treatment (n = 3). Data are expressed as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Scale bar: 50 μm.

Article Snippet: An antibody against HSD11B1 (#AF3397) was purchased from R&D Systems (Minneapolis, MN, USA).

Techniques: Staining, Knockdown, Over Expression, Activity Assay

The effect of RELA, MIRI, and EPL on mRNA expression of MR/GR activity regulators. The mRNA levels of glucocorticoid-activating and -inactivating enzymes were monitored in skin from mice treated as in . ( A ) Hsd11b1 mRNA expression was not significantly altered by RELA, MIRI, or EPL treatment. ( B ) Hsd11b2 mRNA expression was not significantly altered by RELA, MIRI, or EPL treatment. n = 7–8.

Journal: International Journal of Molecular Sciences

Article Title: The Effect of Glucocorticoid and Mineralocorticoid Receptor Antagonists in the Skin of Aged Female Mice

doi: 10.3390/ijms26178346

Figure Lengend Snippet: The effect of RELA, MIRI, and EPL on mRNA expression of MR/GR activity regulators. The mRNA levels of glucocorticoid-activating and -inactivating enzymes were monitored in skin from mice treated as in . ( A ) Hsd11b1 mRNA expression was not significantly altered by RELA, MIRI, or EPL treatment. ( B ) Hsd11b2 mRNA expression was not significantly altered by RELA, MIRI, or EPL treatment. n = 7–8.

Article Snippet: Hsd11b1 , ThermoFisher Scientific , Mm00476182_m1.

Techniques: Expressing, Activity Assay