polyclonal anti human akr1b10  (Boster Bio)

Journal: bioRxiv

Article Title: Akr1b7 functions as a master regulator in ovarian aging

doi: 10.1101/2023.08.09.552567

Figure Lengend Snippet: (A) Quantitative PCR analysis of Akr1b7 mRNA expression was conducted using ovaries collected from YNG and OLD female mice at the indicated time after PMSG/hCG injection. Violin plots show the expression level relative to Gapdh . n = 4–7, **P < 0.01, ***P < 0.001; two-way ANOVA followed by Tukey’s multiple comparisons test. (B) Images show immunohistochemical staining with anti-human AKR1B10 antibody having identical epitope sequence for AKR1B7 in the ovaries of YNG and OLD female mice at the indicated time after PMSG/hCG injection. The sections were incubated with the antibody and were detected with a DAB reaction. Images of stained section were pseudocolored with DAB stains (red), and with hematoxylin counterstains (blue). Circle with dotted lines represents the theca layer. n = 3, Scale bars (white line), 100 µm. (C) Mean intensities of the staining in theca cell layer in were calculated by dividing the signal intensity by the area. Number of follicles was 5–26. n = 3, *P < 0.05, ****P < 0.0001; 2-way ANOVA followed by Tukey’s multiple comparisons test. (D) Violin plots show expressions of AKR1B superfamily genes determined using whole transcriptome analysis. n = 3. (E) Violin plots show Akr1b7 and Akr1b8 mRNA relative expression to Actb in laser micro-dissected theca cell and granulosa cell layer of YNG and OLD female mice. Vim and Amh mRNA were measured as a marker gene of theca and granulosa, respectively. n = 3–6, *P < 0.05, **P < 0.01; two-tailed Student’s t test. (F) Violin plots show Akr1b7 and Akr1b8 mRNA relative expressions to Actb in theca layers of YNG and OLD. *P < 0.05; two-tailed Student’s t test. (G) Lineweaver-Burk plot was determined from the reductase activities for ICA (left panel) or 4-HNE (right panel) in YNG ovary at 24 h after PMSG/hCG injection. (H) Violin plots show reductase activities for ICA (left panel) or 4-HNE (right panel) in the cytosol extracts of YNG and OLD ovaries at 24 h after PMSG/hCG injection. n = 4, *P < 0.05; two-tailed Student’s t test. (I) PGF 2α concentrations were quantified by ELISA using the ovary homogenates of YNG and OLD at 24 h after PMSG/hCG injection. n = 7, **P < 0.01; two-tailed Student’s t test. (J) mRNA expression levels of the indicated Akr1b superfamily were plotted against the PGF 2α concentration in YNG (red) and OLD (blue). n = 7; r indicates Pearson correlation coefficient.

Article Snippet: Sections were immunostained, reacted with 3,3′-diaminobenzidine (DAB) chromogen, and counterstained with hematoxylin as previously described., Primary antibodies used for immunohistochemistry were anti-human AKR1B10 rabbit polyclonal antibody with an identical epitope sequence against mouse AKR1B7 (Thermo Fisher Scientific, #PA5-22036, 1:1500) and anti-DNA/RNA damage mouse monoclonal antibody (Abcam, Cambridge, UK, ab62623, 1:2000).

Techniques: Real-time Polymerase Chain Reaction, Expressing, Injection, Immunohistochemical staining, Staining, Sequencing, Incubation, Marker, Two Tailed Test, Enzyme-linked Immunosorbent Assay, Concentration Assay

Journal: Aging (Albany NY)

Article Title: Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway

doi: 10.18632/aging.103393

Figure Lengend Snippet: Expression of AKR1B10 in CRC tissues. ( A ) Representative IHC images showing in situ AKR1B10 expression in CRC and normal tissues (scale bar = 100μm). ( B – E ) IHC scores of AKR1B10 in ( B ) CRC vs normal tissues, ( C ) T I-II vs T III-IV tissues, ( D ) tumors with or without lymph node invasion, and ( E ) early vs late TNM staging. ( F ) OS of AKR1B10 pos and AKRiB10 neg CRC patients in subgroups demarcated by tumor location, depth of tumor invasion, lymph node metastasis, degree of differentiation and TNM staging. ( G – I ) OS of ( G ) AKR1B10 pos and AKRiB10 neg CRC patients with TNM staging I-II ( H ) and III-IV ( I ). CRC, colorectal cancer. OS, overall survival. ns, no significant difference. ** P < 0.01, *** P < 0.001.

Article Snippet: The processed sections were then blocked with 10% goat serum for 30 min, and incubated overnight with 1:200 diluted polyclonal anti-human AKR1B10 (BOSTER, Wuhan, China) or anti-human FGF1 (BOSTER, Wuhan, China) at 4°C.

Techniques: Expressing, In Situ

Journal: Aging (Albany NY)

Article Title: Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway

doi: 10.18632/aging.103393

Figure Lengend Snippet: Relationship between AKR1B10 and clinic-pathological factors in 135 CRC patients.

Article Snippet: The processed sections were then blocked with 10% goat serum for 30 min, and incubated overnight with 1:200 diluted polyclonal anti-human AKR1B10 (BOSTER, Wuhan, China) or anti-human FGF1 (BOSTER, Wuhan, China) at 4°C.

Techniques:

Journal: Aging (Albany NY)

Article Title: Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway

doi: 10.18632/aging.103393

Figure Lengend Snippet: Results of univariate and multivariate analyses of postoperative patients’ survival by Cox’s proportional hazard model.

Article Snippet: The processed sections were then blocked with 10% goat serum for 30 min, and incubated overnight with 1:200 diluted polyclonal anti-human AKR1B10 (BOSTER, Wuhan, China) or anti-human FGF1 (BOSTER, Wuhan, China) at 4°C.

Techniques: Expressing

Journal: Aging (Albany NY)

Article Title: Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway

doi: 10.18632/aging.103393

Figure Lengend Snippet: Effect of AKR1B10 on CRC cell proliferation and migration ability. ( A ) Comparison of AKR1B10 mRNA expression in CRC and normal tissues across 7 Oncomine datasets. ( B – C ) AKR1B10 mRNA levels in ( B ) 27 paired CRC and normal tissues and ( C ) 5 CRC cell lines. ( D – E ) Immunoblots showing AKR1B10 protein levels in ( D ) wild type and ( E ) AKR1B10-KD and AKR1B10-OE CRC cell lines. ( F – H ) Proliferation rates ( F ), colony forming capacity ( G ) and migration rates ( H ) of AKR1B10-KD and AKR1B10-OE CRC cells. CRC, colorectal cancer. CTL, control; NC, negative control; KD, AKR1B10-shRNA; VEC, vector; OE, AKR1B10 overexpression plasmid. Data are presented as mean ± SD (n=3). * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The processed sections were then blocked with 10% goat serum for 30 min, and incubated overnight with 1:200 diluted polyclonal anti-human AKR1B10 (BOSTER, Wuhan, China) or anti-human FGF1 (BOSTER, Wuhan, China) at 4°C.

Techniques: Migration, Comparison, Expressing, Western Blot, Control, Negative Control, shRNA, Plasmid Preparation, Over Expression

Journal: Aging (Albany NY)

Article Title: Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway

doi: 10.18632/aging.103393

Figure Lengend Snippet: Correlation between AKR1B10 and FGF1 in CRC tissues. ( A ) Correlation analysis of AKR1B10 and FGF1 levels in CRC tissues from TCGA datasets by GEPIA platform. ( B ) FGF1 mRNA levels in 27 paired CRC and normal tissues. ( C ) Correlation between AKR1B10 and FGF1 levels in the above. ( D ) Representative IHC images showing in situ FGF1 expression in CRC and normal tissues (scale bar = 100μm) and ( E ) corresponding IHC scores. ( F ) OS of 135 CRC patients demarcated by FGF1 expression levels. ( G ) Stratification of 135 pairs of CRC and normal tissues into cluster 1 (red) and cluster 2 (green) according to AKR1B10 and FGF1 IHC scores. ( H ) Percentage of tumor and normal samples in each cluster. CRC, colorectal cancer. OS, overall survival. *** P < 0.001.

Article Snippet: The processed sections were then blocked with 10% goat serum for 30 min, and incubated overnight with 1:200 diluted polyclonal anti-human AKR1B10 (BOSTER, Wuhan, China) or anti-human FGF1 (BOSTER, Wuhan, China) at 4°C.

Techniques: In Situ, Expressing

Journal: Aging (Albany NY)

Article Title: Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway

doi: 10.18632/aging.103393

Figure Lengend Snippet: AKR1B10 knockdown suppresses CRC tumor growth in vivo . ( A – B ) Total body weight ( A ) and tumor volume ( B ) of the mice during the experiment. ( C ) Representative pictures of subcutaneous tumors harvested from NC and AKR1B10-KD group. ( D ) The weights of tumor masses. ( E ) Net body weight after subtracting the respective tumor weights. ( F – G ) Relative AKR1B10 ( F ) and FGF1 ( G ) mRNA levels in the tumors and their ( H ) correlation. ( I ) Stratification of mice into cluster 1 (grey) and cluster 2 (blue) according to body weight, tumor volume, tumor weight and AKR1B10 and FGF1 mRNA levels. ( J ) Percentage of NC and AKR1B10-KD mice in each cluster. Data are presented as mean ± SD. CRC, colorectal cancer. NC, negative control; KD, AKR1B10-shRNA. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The processed sections were then blocked with 10% goat serum for 30 min, and incubated overnight with 1:200 diluted polyclonal anti-human AKR1B10 (BOSTER, Wuhan, China) or anti-human FGF1 (BOSTER, Wuhan, China) at 4°C.

Techniques: Knockdown, In Vivo, Negative Control, shRNA

Journal: Aging (Albany NY)

Article Title: Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway

doi: 10.18632/aging.103393

Figure Lengend Snippet: AKR1B10 inhibits CRC cell growth in an FGF1-dependent manner. ( A ) Immunoblot showing AKR1B10, FGF1 and GAPDH protein levels in HT29 cells transfected with AKR1B10-shRNA and in HCT116 cells transfected with AKR1B10 overexpression plasmid. ( B ) Immunoblot showing AKR1B10, FGF1 and GAPDH protein levels in HT29 transfected with FGF1-shRNA alone or in combination with AKR1B10-shRNA. ( C – E ) Proliferation rates ( C ), colony forming capacity ( D ) and migration rates ( E ) of the HT29 cells transfected as above. Data are presented as mean ± SD. NC, negative control; KD, AKR1B10-shRNA; VEC, vector; OE, AKR1B10 overexpression plasmid. “-”, control-shRNA. “+”, AKR1B10 or FGF1 shRNA. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The processed sections were then blocked with 10% goat serum for 30 min, and incubated overnight with 1:200 diluted polyclonal anti-human AKR1B10 (BOSTER, Wuhan, China) or anti-human FGF1 (BOSTER, Wuhan, China) at 4°C.

Techniques: Western Blot, Transfection, shRNA, Over Expression, Plasmid Preparation, Migration, Negative Control, Control

Journal: Human pathology

Article Title: Aldo-Ketoreductase Family 1 B10 (AKR1B10) as A Biomarker to Distinguish Hepatocellular Carcinoma from Benign Liver Lesions

doi: 10.1016/j.humpath.2013.12.002

Figure Lengend Snippet: Table 2

Article Snippet: 35µg of protein was loaded on a 10% SDS-polyacrylamide gel and transferred to a Immun-Blot PVDF Membrane (BioRad, Hercules, CA), blocked using 1X TBST containing 0.05% Tween-20 and 5% non-fat powdered milk, followed by membrane incubation with polyclonal rabbit anti-human AKR1B10 primary antibody (1:300; LifeSpan BioSciences, Inc., Seattle, WA) solution overnight at 4°C.

Techniques: