A05668 Search Results


rabbit anti somatostatin  (Agilent technologies)
90
Agilent technologies rabbit anti somatostatin
Rabbit Anti Somatostatin, supplied by Agilent technologies, 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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rabbit anti-somatostatin  (Agilent technologies)
90
Agilent technologies rabbit anti-somatostatin
Cdk4 controls β cell proliferation and mass during embryogenesis. (A-D) At P1, BrdU+ Ins+ cells are not observed (‡) in Cdk4−/− pancreas (B,D), whereas numbers are increased in Cdk4R24C (C,D) as compared with Cdk4+/+ (A,D) pancreas. Arrows indicate BrdU+ Ins+ cells. (D) Percentage of BrdU+ Ins+ cells in total Ins+ cells. (E) Cdk4 deficiency results in a reduced β cell mass and the Cdk4R24C pancreas shows a significant increase in β cell mass as compared with Cdk4+/+ pancreas at P1. (F-I) Numbers of insulin-expressing β cells are reduced in Cdk4−/− (G,I) and increased in Cdk4R24C (H,I) as compared with Cdk4+/+ (F,I) pancreas at P1. The numbers of non-β cells expressing glucagon, <t>somatostatin</t> and pancreatic polypeptide (Ppy) are comparable in the islets of all genotypes. (I) The numbers of cells in islets from P1 mice of all three genotypes expressing insulin (closed circles) or non-β cell hormones (glucagon, somatostatin and Ppy, open circles) are shown. (J) Real-time PCR detection of Ngn3 transcripts from embryonic (E12.5 and E14.5), postnatal (P1) pancreases and fetal pancreatic (FP) cells (after 3 days of culture) from Cdk4+/+, Cdk4−/− and Cdk4R24C pancreas. Ngn3 transcripts are undetectable (‡) in FP cells from Cdk4−/− mice. Fold change is relative to expression in Cdk4+/+. (K,L) Detection of Ngn3+ cells at P1 in Cdk4R24C pancreas (L, circled) but not Cdk4+/+ pancreas (K). *, P<0.05; **, P<0.001; Student's t-test. Error bars indicate s.e.m. Scale bars: 50 μm.
Rabbit Anti Somatostatin, supplied by Agilent technologies, 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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Average 90 stars, based on 1 article reviews
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goat anti-mouse igg  (Beyotime)
90
Beyotime goat anti-mouse igg
Cdk4 controls β cell proliferation and mass during embryogenesis. (A-D) At P1, BrdU+ Ins+ cells are not observed (‡) in Cdk4−/− pancreas (B,D), whereas numbers are increased in Cdk4R24C (C,D) as compared with Cdk4+/+ (A,D) pancreas. Arrows indicate BrdU+ Ins+ cells. (D) Percentage of BrdU+ Ins+ cells in total Ins+ cells. (E) Cdk4 deficiency results in a reduced β cell mass and the Cdk4R24C pancreas shows a significant increase in β cell mass as compared with Cdk4+/+ pancreas at P1. (F-I) Numbers of insulin-expressing β cells are reduced in Cdk4−/− (G,I) and increased in Cdk4R24C (H,I) as compared with Cdk4+/+ (F,I) pancreas at P1. The numbers of non-β cells expressing glucagon, <t>somatostatin</t> and pancreatic polypeptide (Ppy) are comparable in the islets of all genotypes. (I) The numbers of cells in islets from P1 mice of all three genotypes expressing insulin (closed circles) or non-β cell hormones (glucagon, somatostatin and Ppy, open circles) are shown. (J) Real-time PCR detection of Ngn3 transcripts from embryonic (E12.5 and E14.5), postnatal (P1) pancreases and fetal pancreatic (FP) cells (after 3 days of culture) from Cdk4+/+, Cdk4−/− and Cdk4R24C pancreas. Ngn3 transcripts are undetectable (‡) in FP cells from Cdk4−/− mice. Fold change is relative to expression in Cdk4+/+. (K,L) Detection of Ngn3+ cells at P1 in Cdk4R24C pancreas (L, circled) but not Cdk4+/+ pancreas (K). *, P<0.05; **, P<0.001; Student's t-test. Error bars indicate s.e.m. Scale bars: 50 μm.
Goat Anti Mouse Igg, supplied by Beyotime, 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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a0566  (Santa Cruz Biotechnology)
96
Santa Cruz Biotechnology a0566
Cdk4 controls β cell proliferation and mass during embryogenesis. (A-D) At P1, BrdU+ Ins+ cells are not observed (‡) in Cdk4−/− pancreas (B,D), whereas numbers are increased in Cdk4R24C (C,D) as compared with Cdk4+/+ (A,D) pancreas. Arrows indicate BrdU+ Ins+ cells. (D) Percentage of BrdU+ Ins+ cells in total Ins+ cells. (E) Cdk4 deficiency results in a reduced β cell mass and the Cdk4R24C pancreas shows a significant increase in β cell mass as compared with Cdk4+/+ pancreas at P1. (F-I) Numbers of insulin-expressing β cells are reduced in Cdk4−/− (G,I) and increased in Cdk4R24C (H,I) as compared with Cdk4+/+ (F,I) pancreas at P1. The numbers of non-β cells expressing glucagon, <t>somatostatin</t> and pancreatic polypeptide (Ppy) are comparable in the islets of all genotypes. (I) The numbers of cells in islets from P1 mice of all three genotypes expressing insulin (closed circles) or non-β cell hormones (glucagon, somatostatin and Ppy, open circles) are shown. (J) Real-time PCR detection of Ngn3 transcripts from embryonic (E12.5 and E14.5), postnatal (P1) pancreases and fetal pancreatic (FP) cells (after 3 days of culture) from Cdk4+/+, Cdk4−/− and Cdk4R24C pancreas. Ngn3 transcripts are undetectable (‡) in FP cells from Cdk4−/− mice. Fold change is relative to expression in Cdk4+/+. (K,L) Detection of Ngn3+ cells at P1 in Cdk4R24C pancreas (L, circled) but not Cdk4+/+ pancreas (K). *, P<0.05; **, P<0.001; Student's t-test. Error bars indicate s.e.m. Scale bars: 50 μm.
A0566, supplied by Santa Cruz Biotechnology, 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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somatostatin  (Agilent technologies)
90
Agilent technologies somatostatin
Cdk4 controls β cell proliferation and mass during embryogenesis. (A-D) At P1, BrdU+ Ins+ cells are not observed (‡) in Cdk4−/− pancreas (B,D), whereas numbers are increased in Cdk4R24C (C,D) as compared with Cdk4+/+ (A,D) pancreas. Arrows indicate BrdU+ Ins+ cells. (D) Percentage of BrdU+ Ins+ cells in total Ins+ cells. (E) Cdk4 deficiency results in a reduced β cell mass and the Cdk4R24C pancreas shows a significant increase in β cell mass as compared with Cdk4+/+ pancreas at P1. (F-I) Numbers of insulin-expressing β cells are reduced in Cdk4−/− (G,I) and increased in Cdk4R24C (H,I) as compared with Cdk4+/+ (F,I) pancreas at P1. The numbers of non-β cells expressing glucagon, <t>somatostatin</t> and pancreatic polypeptide (Ppy) are comparable in the islets of all genotypes. (I) The numbers of cells in islets from P1 mice of all three genotypes expressing insulin (closed circles) or non-β cell hormones (glucagon, somatostatin and Ppy, open circles) are shown. (J) Real-time PCR detection of Ngn3 transcripts from embryonic (E12.5 and E14.5), postnatal (P1) pancreases and fetal pancreatic (FP) cells (after 3 days of culture) from Cdk4+/+, Cdk4−/− and Cdk4R24C pancreas. Ngn3 transcripts are undetectable (‡) in FP cells from Cdk4−/− mice. Fold change is relative to expression in Cdk4+/+. (K,L) Detection of Ngn3+ cells at P1 in Cdk4R24C pancreas (L, circled) but not Cdk4+/+ pancreas (K). *, P<0.05; **, P<0.001; Student's t-test. Error bars indicate s.e.m. Scale bars: 50 μm.
Somatostatin, supplied by Agilent technologies, 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/somatostatin/product/Agilent technologies
Average 90 stars, based on 1 article reviews
somatostatin - by Bioz Stars, 2026-05
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podxl  (Boster Bio)
91
Boster Bio podxl
Cdk4 controls β cell proliferation and mass during embryogenesis. (A-D) At P1, BrdU+ Ins+ cells are not observed (‡) in Cdk4−/− pancreas (B,D), whereas numbers are increased in Cdk4R24C (C,D) as compared with Cdk4+/+ (A,D) pancreas. Arrows indicate BrdU+ Ins+ cells. (D) Percentage of BrdU+ Ins+ cells in total Ins+ cells. (E) Cdk4 deficiency results in a reduced β cell mass and the Cdk4R24C pancreas shows a significant increase in β cell mass as compared with Cdk4+/+ pancreas at P1. (F-I) Numbers of insulin-expressing β cells are reduced in Cdk4−/− (G,I) and increased in Cdk4R24C (H,I) as compared with Cdk4+/+ (F,I) pancreas at P1. The numbers of non-β cells expressing glucagon, <t>somatostatin</t> and pancreatic polypeptide (Ppy) are comparable in the islets of all genotypes. (I) The numbers of cells in islets from P1 mice of all three genotypes expressing insulin (closed circles) or non-β cell hormones (glucagon, somatostatin and Ppy, open circles) are shown. (J) Real-time PCR detection of Ngn3 transcripts from embryonic (E12.5 and E14.5), postnatal (P1) pancreases and fetal pancreatic (FP) cells (after 3 days of culture) from Cdk4+/+, Cdk4−/− and Cdk4R24C pancreas. Ngn3 transcripts are undetectable (‡) in FP cells from Cdk4−/− mice. Fold change is relative to expression in Cdk4+/+. (K,L) Detection of Ngn3+ cells at P1 in Cdk4R24C pancreas (L, circled) but not Cdk4+/+ pancreas (K). *, P<0.05; **, P<0.001; Student's t-test. Error bars indicate s.e.m. Scale bars: 50 μm.
Podxl, supplied by Boster Bio, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/podxl/product/Boster Bio
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rabbit anti-gastrin antibody  (Agilent technologies)
90
Agilent technologies rabbit anti-gastrin antibody
Cdk4 controls β cell proliferation and mass during embryogenesis. (A-D) At P1, BrdU+ Ins+ cells are not observed (‡) in Cdk4−/− pancreas (B,D), whereas numbers are increased in Cdk4R24C (C,D) as compared with Cdk4+/+ (A,D) pancreas. Arrows indicate BrdU+ Ins+ cells. (D) Percentage of BrdU+ Ins+ cells in total Ins+ cells. (E) Cdk4 deficiency results in a reduced β cell mass and the Cdk4R24C pancreas shows a significant increase in β cell mass as compared with Cdk4+/+ pancreas at P1. (F-I) Numbers of insulin-expressing β cells are reduced in Cdk4−/− (G,I) and increased in Cdk4R24C (H,I) as compared with Cdk4+/+ (F,I) pancreas at P1. The numbers of non-β cells expressing glucagon, <t>somatostatin</t> and pancreatic polypeptide (Ppy) are comparable in the islets of all genotypes. (I) The numbers of cells in islets from P1 mice of all three genotypes expressing insulin (closed circles) or non-β cell hormones (glucagon, somatostatin and Ppy, open circles) are shown. (J) Real-time PCR detection of Ngn3 transcripts from embryonic (E12.5 and E14.5), postnatal (P1) pancreases and fetal pancreatic (FP) cells (after 3 days of culture) from Cdk4+/+, Cdk4−/− and Cdk4R24C pancreas. Ngn3 transcripts are undetectable (‡) in FP cells from Cdk4−/− mice. Fold change is relative to expression in Cdk4+/+. (K,L) Detection of Ngn3+ cells at P1 in Cdk4R24C pancreas (L, circled) but not Cdk4+/+ pancreas (K). *, P<0.05; **, P<0.001; Student's t-test. Error bars indicate s.e.m. Scale bars: 50 μm.
Rabbit Anti Gastrin Antibody, supplied by Agilent technologies, 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/rabbit anti-gastrin antibody/product/Agilent technologies
Average 90 stars, based on 1 article reviews
rabbit anti-gastrin antibody - by Bioz Stars, 2026-05
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goat anti-rabbit fitc-conjugated igg #a0568  (Beyotime)
90
Beyotime goat anti-rabbit fitc-conjugated igg #a0568
Cdk4 controls β cell proliferation and mass during embryogenesis. (A-D) At P1, BrdU+ Ins+ cells are not observed (‡) in Cdk4−/− pancreas (B,D), whereas numbers are increased in Cdk4R24C (C,D) as compared with Cdk4+/+ (A,D) pancreas. Arrows indicate BrdU+ Ins+ cells. (D) Percentage of BrdU+ Ins+ cells in total Ins+ cells. (E) Cdk4 deficiency results in a reduced β cell mass and the Cdk4R24C pancreas shows a significant increase in β cell mass as compared with Cdk4+/+ pancreas at P1. (F-I) Numbers of insulin-expressing β cells are reduced in Cdk4−/− (G,I) and increased in Cdk4R24C (H,I) as compared with Cdk4+/+ (F,I) pancreas at P1. The numbers of non-β cells expressing glucagon, <t>somatostatin</t> and pancreatic polypeptide (Ppy) are comparable in the islets of all genotypes. (I) The numbers of cells in islets from P1 mice of all three genotypes expressing insulin (closed circles) or non-β cell hormones (glucagon, somatostatin and Ppy, open circles) are shown. (J) Real-time PCR detection of Ngn3 transcripts from embryonic (E12.5 and E14.5), postnatal (P1) pancreases and fetal pancreatic (FP) cells (after 3 days of culture) from Cdk4+/+, Cdk4−/− and Cdk4R24C pancreas. Ngn3 transcripts are undetectable (‡) in FP cells from Cdk4−/− mice. Fold change is relative to expression in Cdk4+/+. (K,L) Detection of Ngn3+ cells at P1 in Cdk4R24C pancreas (L, circled) but not Cdk4+/+ pancreas (K). *, P<0.05; **, P<0.001; Student's t-test. Error bars indicate s.e.m. Scale bars: 50 μm.
Goat Anti Rabbit Fitc Conjugated Igg #A0568, supplied by Beyotime, 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/goat anti-rabbit fitc-conjugated igg #a0568/product/Beyotime
Average 90 stars, based on 1 article reviews
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secondary antibodies alexa fluor555-labeled donkey anti-rabbit igg  (Beyotime)
90
Beyotime secondary antibodies alexa fluor555-labeled donkey anti-rabbit igg
Cdk4 controls β cell proliferation and mass during embryogenesis. (A-D) At P1, BrdU+ Ins+ cells are not observed (‡) in Cdk4−/− pancreas (B,D), whereas numbers are increased in Cdk4R24C (C,D) as compared with Cdk4+/+ (A,D) pancreas. Arrows indicate BrdU+ Ins+ cells. (D) Percentage of BrdU+ Ins+ cells in total Ins+ cells. (E) Cdk4 deficiency results in a reduced β cell mass and the Cdk4R24C pancreas shows a significant increase in β cell mass as compared with Cdk4+/+ pancreas at P1. (F-I) Numbers of insulin-expressing β cells are reduced in Cdk4−/− (G,I) and increased in Cdk4R24C (H,I) as compared with Cdk4+/+ (F,I) pancreas at P1. The numbers of non-β cells expressing glucagon, <t>somatostatin</t> and pancreatic polypeptide (Ppy) are comparable in the islets of all genotypes. (I) The numbers of cells in islets from P1 mice of all three genotypes expressing insulin (closed circles) or non-β cell hormones (glucagon, somatostatin and Ppy, open circles) are shown. (J) Real-time PCR detection of Ngn3 transcripts from embryonic (E12.5 and E14.5), postnatal (P1) pancreases and fetal pancreatic (FP) cells (after 3 days of culture) from Cdk4+/+, Cdk4−/− and Cdk4R24C pancreas. Ngn3 transcripts are undetectable (‡) in FP cells from Cdk4−/− mice. Fold change is relative to expression in Cdk4+/+. (K,L) Detection of Ngn3+ cells at P1 in Cdk4R24C pancreas (L, circled) but not Cdk4+/+ pancreas (K). *, P<0.05; **, P<0.001; Student's t-test. Error bars indicate s.e.m. Scale bars: 50 μm.
Secondary Antibodies Alexa Fluor555 Labeled Donkey Anti Rabbit Igg, supplied by Beyotime, 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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mmp1  (Boster Bio)
94
Boster Bio mmp1
OTUD6B−AS1 was associated with aggressive pathological parameters and promoted breast cancer progression. Expression of OTUD6B−AS1 was positively correlated with axillary lymph node metastasis ( A ), larger tumor size ( B ), advanced tumor stage ( C , one way ANOVA, P = 0.0096; stage I vs. II, P = 0.0050; stage I vs. III, P = 0.0162; stage II vs. III, not significant), and high Ki-67 expression ( D ). The OTUD6B−AS1 overexpression plasmid significantly upregulated OTUD6B−AS1 expression in breast cancer BT474 cells ( E ). OTUD6B−AS1 promoted breast cancer cell proliferation ( F ), wound healing ( G , 40× magnification), migration, and invasion ( H , I , 200× magnification). OTUD6B−AS1 increased the tube formation ability of HUVEC ( J , 40× magnification). OTUD6B−AS1 decreased E-cadherin expression and increased the expression of HIF-1α, <t>MMP1,</t> SMAD5, Snail, Twist1, and VEGFA ( K , cropped gels blots are used).
Mmp1, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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2,2′-azobis(isobutyronitrile) aibn  (Tokyo Chemical Industry)
90
Tokyo Chemical Industry 2,2′-azobis(isobutyronitrile) aibn
OTUD6B−AS1 was associated with aggressive pathological parameters and promoted breast cancer progression. Expression of OTUD6B−AS1 was positively correlated with axillary lymph node metastasis ( A ), larger tumor size ( B ), advanced tumor stage ( C , one way ANOVA, P = 0.0096; stage I vs. II, P = 0.0050; stage I vs. III, P = 0.0162; stage II vs. III, not significant), and high Ki-67 expression ( D ). The OTUD6B−AS1 overexpression plasmid significantly upregulated OTUD6B−AS1 expression in breast cancer BT474 cells ( E ). OTUD6B−AS1 promoted breast cancer cell proliferation ( F ), wound healing ( G , 40× magnification), migration, and invasion ( H , I , 200× magnification). OTUD6B−AS1 increased the tube formation ability of HUVEC ( J , 40× magnification). OTUD6B−AS1 decreased E-cadherin expression and increased the expression of HIF-1α, <t>MMP1,</t> SMAD5, Snail, Twist1, and VEGFA ( K , cropped gels blots are used).
2,2′ Azobis(isobutyronitrile) Aibn, supplied by Tokyo Chemical Industry, 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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Image Search Results


Cdk4 controls β cell proliferation and mass during embryogenesis. (A-D) At P1, BrdU+ Ins+ cells are not observed (‡) in Cdk4−/− pancreas (B,D), whereas numbers are increased in Cdk4R24C (C,D) as compared with Cdk4+/+ (A,D) pancreas. Arrows indicate BrdU+ Ins+ cells. (D) Percentage of BrdU+ Ins+ cells in total Ins+ cells. (E) Cdk4 deficiency results in a reduced β cell mass and the Cdk4R24C pancreas shows a significant increase in β cell mass as compared with Cdk4+/+ pancreas at P1. (F-I) Numbers of insulin-expressing β cells are reduced in Cdk4−/− (G,I) and increased in Cdk4R24C (H,I) as compared with Cdk4+/+ (F,I) pancreas at P1. The numbers of non-β cells expressing glucagon, somatostatin and pancreatic polypeptide (Ppy) are comparable in the islets of all genotypes. (I) The numbers of cells in islets from P1 mice of all three genotypes expressing insulin (closed circles) or non-β cell hormones (glucagon, somatostatin and Ppy, open circles) are shown. (J) Real-time PCR detection of Ngn3 transcripts from embryonic (E12.5 and E14.5), postnatal (P1) pancreases and fetal pancreatic (FP) cells (after 3 days of culture) from Cdk4+/+, Cdk4−/− and Cdk4R24C pancreas. Ngn3 transcripts are undetectable (‡) in FP cells from Cdk4−/− mice. Fold change is relative to expression in Cdk4+/+. (K,L) Detection of Ngn3+ cells at P1 in Cdk4R24C pancreas (L, circled) but not Cdk4+/+ pancreas (K). *, P<0.05; **, P<0.001; Student's t-test. Error bars indicate s.e.m. Scale bars: 50 μm.

Journal: Development (Cambridge, England)

Article Title: The Cdk4-E2f1 pathway regulates early pancreas development by targeting Pdx1 + progenitors and Ngn3 + endocrine precursors

doi: 10.1242/dev.061481

Figure Lengend Snippet: Cdk4 controls β cell proliferation and mass during embryogenesis. (A-D) At P1, BrdU+ Ins+ cells are not observed (‡) in Cdk4−/− pancreas (B,D), whereas numbers are increased in Cdk4R24C (C,D) as compared with Cdk4+/+ (A,D) pancreas. Arrows indicate BrdU+ Ins+ cells. (D) Percentage of BrdU+ Ins+ cells in total Ins+ cells. (E) Cdk4 deficiency results in a reduced β cell mass and the Cdk4R24C pancreas shows a significant increase in β cell mass as compared with Cdk4+/+ pancreas at P1. (F-I) Numbers of insulin-expressing β cells are reduced in Cdk4−/− (G,I) and increased in Cdk4R24C (H,I) as compared with Cdk4+/+ (F,I) pancreas at P1. The numbers of non-β cells expressing glucagon, somatostatin and pancreatic polypeptide (Ppy) are comparable in the islets of all genotypes. (I) The numbers of cells in islets from P1 mice of all three genotypes expressing insulin (closed circles) or non-β cell hormones (glucagon, somatostatin and Ppy, open circles) are shown. (J) Real-time PCR detection of Ngn3 transcripts from embryonic (E12.5 and E14.5), postnatal (P1) pancreases and fetal pancreatic (FP) cells (after 3 days of culture) from Cdk4+/+, Cdk4−/− and Cdk4R24C pancreas. Ngn3 transcripts are undetectable (‡) in FP cells from Cdk4−/− mice. Fold change is relative to expression in Cdk4+/+. (K,L) Detection of Ngn3+ cells at P1 in Cdk4R24C pancreas (L, circled) but not Cdk4+/+ pancreas (K). *, P<0.05; **, P<0.001; Student's t-test. Error bars indicate s.e.m. Scale bars: 50 μm.

Article Snippet: Mouse tissues were harvested, paraffin sectioned and immunostained overnight at 4°C with the following primary antibodies: goat anti-Pdx1 (ab47383, Abcam), rabbit anti-Pdx1 (AB3503, Millipore), goat anti-vimentin (AB1620, Millipore), mouse anti-Ngn3 (F25A1B3, DSHB at University of Iowa), mouse anti-Isl1 (40.2D6, DSHB), mouse anti-Nkx2.2 (74.5A5, DSHB), mouse anti-Nkx6.1 (F64A6B4, DSHB), mouse anti-E-cadherin (610181, BD Biosciences), rabbit anti-Cdk4 (sc-260, Santa Cruz), rabbit anti-E2f1 (ab94888, Abcam), guinea pig anti-insulin (A0564, Dako), rabbit anti-glucagon (A0565, Dako), rabbit anti-somatostatin (A0566, Dako), goat anti-pancreatic polypeptide (Ppy; EB06805, Everest Biotech), rabbit anti-Ki67 (NCL-Ki67p, Leica) and mouse anti-BrdU (M0744, Dako).

Techniques: Expressing, Real-time Polymerase Chain Reaction

OTUD6B−AS1 was associated with aggressive pathological parameters and promoted breast cancer progression. Expression of OTUD6B−AS1 was positively correlated with axillary lymph node metastasis ( A ), larger tumor size ( B ), advanced tumor stage ( C , one way ANOVA, P = 0.0096; stage I vs. II, P = 0.0050; stage I vs. III, P = 0.0162; stage II vs. III, not significant), and high Ki-67 expression ( D ). The OTUD6B−AS1 overexpression plasmid significantly upregulated OTUD6B−AS1 expression in breast cancer BT474 cells ( E ). OTUD6B−AS1 promoted breast cancer cell proliferation ( F ), wound healing ( G , 40× magnification), migration, and invasion ( H , I , 200× magnification). OTUD6B−AS1 increased the tube formation ability of HUVEC ( J , 40× magnification). OTUD6B−AS1 decreased E-cadherin expression and increased the expression of HIF-1α, MMP1, SMAD5, Snail, Twist1, and VEGFA ( K , cropped gels blots are used).

Journal: Aging (Albany NY)

Article Title: An angiogenesis-related lncRNA signature predicts the immune microenvironment and prognosis of breast cancer

doi: 10.18632/aging.204930

Figure Lengend Snippet: OTUD6B−AS1 was associated with aggressive pathological parameters and promoted breast cancer progression. Expression of OTUD6B−AS1 was positively correlated with axillary lymph node metastasis ( A ), larger tumor size ( B ), advanced tumor stage ( C , one way ANOVA, P = 0.0096; stage I vs. II, P = 0.0050; stage I vs. III, P = 0.0162; stage II vs. III, not significant), and high Ki-67 expression ( D ). The OTUD6B−AS1 overexpression plasmid significantly upregulated OTUD6B−AS1 expression in breast cancer BT474 cells ( E ). OTUD6B−AS1 promoted breast cancer cell proliferation ( F ), wound healing ( G , 40× magnification), migration, and invasion ( H , I , 200× magnification). OTUD6B−AS1 increased the tube formation ability of HUVEC ( J , 40× magnification). OTUD6B−AS1 decreased E-cadherin expression and increased the expression of HIF-1α, MMP1, SMAD5, Snail, Twist1, and VEGFA ( K , cropped gels blots are used).

Article Snippet: For the western blot analysis, the antibodies used were as follows: E-cadherin (AF0131, 1:1000, Affinity), VEGFA (sc-57496, 1:200, Santa Cruz), SMAD5 (ab40771, 1:5000, Abcam), MMP1 (A0568, 1:1000, Boster), HIF1α (sc-13515, 1:200, Santa Cruz), Snail (3099-1-AP, 1:1000, Proteintech), and Twist1 (5465-1-AP, 1:1000, Proteintech), with GAPDH (AB0037, 1:5000, Abways) used as an internal control.

Techniques: Expressing, Over Expression, Plasmid Preparation, Migration