5.4 kb mouse ap2 promoter construct Search Results


alkaline phosphatase alp  (Developmental Studies Hybridoma Bank)
93
Developmental Studies Hybridoma Bank alkaline phosphatase alp
Alkaline Phosphatase Alp, supplied by Developmental Studies Hybridoma Bank, 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/result/alkaline phosphatase alp/product/Developmental Studies Hybridoma Bank
Average 93 stars, based on 1 article reviews
alkaline phosphatase alp - by Bioz Stars, 2026-06
93/100 stars
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pgl3-basic  (Promega)
90
Promega pgl3-basic
Pgl3 Basic, supplied by Promega, 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/pgl3-basic/product/Promega
Average 90 stars, based on 1 article reviews
pgl3-basic - by Bioz Stars, 2026-06
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alg5  (Abcam)
99
Abcam alg5
Primer sequences for specific genes.
Alg5, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 99 stars, based on 1 article reviews
alg5 - by Bioz Stars, 2026-06
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Image Search Results


Primer sequences for specific genes.

Journal: Experimental and Therapeutic Medicine

Article Title: miR-4262 regulates chondrocyte viability, apoptosis, autophagy by targeting SIRT1 and activating PI3K/AKT/mTOR signaling pathway in rats with osteoarthritis

doi: 10.3892/etm.2017.5444

Figure Lengend Snippet: Primer sequences for specific genes.

Article Snippet: Total 50 µg protein sample (per lane) was separated on SDS-PAGE gel, blotted onto PVDF membranes, and blocked in 5% non-fat milk for 1 h. The membranes were probed with mouse polyclonal antibodies to ULK1 (120 kDa; 1;1,000; ab128859; Abcam, Cambridge, UK), ALG5 (32 kDa; 1;1,000; ab108327; Abcam), Beclin-1 (52 kDa; 1;1,000; ab62557; Abcam), LC3II/LC3I (LC3-II, 17 kDa, LC3-II 19 kDa; 1;1,000; ab48394; Abcam), COL2A1 (142 kDa; 1;1,000; ab34712; Abcam), ACAN (250 kDa; 1;1,000; ab36861; Abcam), MMP-13 (54 kDa; 1;1,000; ab39012; Abcam), ADAMTS-5 (73 kDa; 1;1,000; ab41037; Abcam), SIRT1 (120 kDa; 1;1,000; ab110304; Abcam), phospho-PI3K (p-PI3K) (84 kDa; 1;1,000; ab182651; Abcam), PI3K (123 kDa; 1;1,000; ab151549; Abcam), p-AKT (65 kDa; 1;1,000; SAB4301414; Sigma-Aldrich; Merck KGaA), AKT (55 kDa; 1;1,000; SAB4500797; Sigma-Aldrich; Merck KGaA), p-mTOR (250 kDa; 1;1,000; ab137133; Abcam), mTOR (252 kDa; 1;2,000; ab2732; Abcam), and GAPDH (36 kDa; 1;2,000; ab8245; Abcam) overnight at 4°C, respectively.

Techniques: Sequencing

TNF-α treatment significantly decreases cell viability and autophagy, as well as increases apoptosis and the expression of miR-4262 in chondrocytes. (A) The cell viability in control and TNF-α groups at 0, 12, 24, 48 h using CCK-8; (B) The cell apoptosis in control and TNF-α groups at 0, 12, 24, 48 h using TUNEL staining; (C) The expression of autophagy-related proteins, including ULK1, ALG5, Beclin-1, LC3II/LC3I, in control, TNF-α, RAPA and TNF-α + E64d + pepstatin A groups using western blotting; (D) The level of miR-4262 in control and TNF-α groups at 0, 12, 24, 48 h using quantitative reverse transcription PCR. Three independent experiments were performed in each assay. *P<0.05, **P<0.01, and ***P<0.001 compared with the control group, #P<0.05 compared with the TNF-α group. TNF-α, tumor necrosis factor-α; RAPA, rapamycin; ULK1, uncoordinated 51-like kinase 1; ALG5, asparagine-linked glycosylation 5.

Journal: Experimental and Therapeutic Medicine

Article Title: miR-4262 regulates chondrocyte viability, apoptosis, autophagy by targeting SIRT1 and activating PI3K/AKT/mTOR signaling pathway in rats with osteoarthritis

doi: 10.3892/etm.2017.5444

Figure Lengend Snippet: TNF-α treatment significantly decreases cell viability and autophagy, as well as increases apoptosis and the expression of miR-4262 in chondrocytes. (A) The cell viability in control and TNF-α groups at 0, 12, 24, 48 h using CCK-8; (B) The cell apoptosis in control and TNF-α groups at 0, 12, 24, 48 h using TUNEL staining; (C) The expression of autophagy-related proteins, including ULK1, ALG5, Beclin-1, LC3II/LC3I, in control, TNF-α, RAPA and TNF-α + E64d + pepstatin A groups using western blotting; (D) The level of miR-4262 in control and TNF-α groups at 0, 12, 24, 48 h using quantitative reverse transcription PCR. Three independent experiments were performed in each assay. *P<0.05, **P<0.01, and ***P<0.001 compared with the control group, #P<0.05 compared with the TNF-α group. TNF-α, tumor necrosis factor-α; RAPA, rapamycin; ULK1, uncoordinated 51-like kinase 1; ALG5, asparagine-linked glycosylation 5.

Article Snippet: Total 50 µg protein sample (per lane) was separated on SDS-PAGE gel, blotted onto PVDF membranes, and blocked in 5% non-fat milk for 1 h. The membranes were probed with mouse polyclonal antibodies to ULK1 (120 kDa; 1;1,000; ab128859; Abcam, Cambridge, UK), ALG5 (32 kDa; 1;1,000; ab108327; Abcam), Beclin-1 (52 kDa; 1;1,000; ab62557; Abcam), LC3II/LC3I (LC3-II, 17 kDa, LC3-II 19 kDa; 1;1,000; ab48394; Abcam), COL2A1 (142 kDa; 1;1,000; ab34712; Abcam), ACAN (250 kDa; 1;1,000; ab36861; Abcam), MMP-13 (54 kDa; 1;1,000; ab39012; Abcam), ADAMTS-5 (73 kDa; 1;1,000; ab41037; Abcam), SIRT1 (120 kDa; 1;1,000; ab110304; Abcam), phospho-PI3K (p-PI3K) (84 kDa; 1;1,000; ab182651; Abcam), PI3K (123 kDa; 1;1,000; ab151549; Abcam), p-AKT (65 kDa; 1;1,000; SAB4301414; Sigma-Aldrich; Merck KGaA), AKT (55 kDa; 1;1,000; SAB4500797; Sigma-Aldrich; Merck KGaA), p-mTOR (250 kDa; 1;1,000; ab137133; Abcam), mTOR (252 kDa; 1;2,000; ab2732; Abcam), and GAPDH (36 kDa; 1;2,000; ab8245; Abcam) overnight at 4°C, respectively.

Techniques: Expressing, CCK-8 Assay, TUNEL Assay, Staining, Western Blot

Upregulated miR-4262 further decreases cell viability, autophagy, and matrix synthesis as well as increases apoptosis in TNF-α-treated chondrocytes. (A) The miR-4262 level in control, scramble (control of mimic), miR-4262 mimic, NC (control of inhibitor), and miR-4262 inhibitor groups by qPCR; (B) The cell viability in control, scramble, miR-4262 mimic, inhibitor NC, and miR-4262 inhibitor groups using CCK-8; (C) The cell apoptosis in control, scramble, miR-4262 mimic, inhibitor NC, and miR-4262 inhibitor groups using TUNEL staining; (D) The expression of autophagy-related proteins, including ULK1, ALG5, Beclin-1, LC3II/LC3I, in control, scramble, miR-4262 mimic, inhibitor NC, and miR-4262 inhibitor groups using western blotting; (E) The cell viability in control, TNF-α, TNF-α + scramble, TNF-α + miR-4262 mimic, TNF-α + NC, and TNF-α + miR-4262 inhibitor groups using CCK-8; (F) The cell apoptosis in control, TNF-α, TNF-α + scramble, TNF-α + miR-4262 mimic, TNF-α + NC, and TNF-α + miR-4262 inhibitor groups using TUNEL staining; (G) The expression of autophagy-related proteins, including ULK1, ALG5, Beclin-1, LC3II/LC3I, in control, TNF-α, TNF-α+E64d+pepstatin (A) TNF-α + scramble, TNF-α + miR-4262 mimic, TNF-α + NC, and TNF-α + miR-4262 inhibitor groups using western blotting; (H) The expression of matrix synthesis-related proteins, such as COL2A1, ACAN, MMP-13 and ADAMTS-5, in control, TNF-α, TNF-α + scramble, TNF-α + miR-4262 mimic, TNF-α + NC, and TNF-α + miR-4262 inhibitor groups using western blotting. Three independent experiments were performed in each assay. *P<0.05, **P<0.01, and ***P<0.001 TNF-α, tumor necrosis factor-α; ULK1, uncoordinated 51-like kinase 1; ALG5, asparagine-linked glycosylation 5; COL2A1, type II collagen; ACAN, aggrecan; MMP-13, matrix metallo protease 13; ADAMTS-5, a disintegrin and metalloproteinase with thrombospondin motifs-5.

Journal: Experimental and Therapeutic Medicine

Article Title: miR-4262 regulates chondrocyte viability, apoptosis, autophagy by targeting SIRT1 and activating PI3K/AKT/mTOR signaling pathway in rats with osteoarthritis

doi: 10.3892/etm.2017.5444

Figure Lengend Snippet: Upregulated miR-4262 further decreases cell viability, autophagy, and matrix synthesis as well as increases apoptosis in TNF-α-treated chondrocytes. (A) The miR-4262 level in control, scramble (control of mimic), miR-4262 mimic, NC (control of inhibitor), and miR-4262 inhibitor groups by qPCR; (B) The cell viability in control, scramble, miR-4262 mimic, inhibitor NC, and miR-4262 inhibitor groups using CCK-8; (C) The cell apoptosis in control, scramble, miR-4262 mimic, inhibitor NC, and miR-4262 inhibitor groups using TUNEL staining; (D) The expression of autophagy-related proteins, including ULK1, ALG5, Beclin-1, LC3II/LC3I, in control, scramble, miR-4262 mimic, inhibitor NC, and miR-4262 inhibitor groups using western blotting; (E) The cell viability in control, TNF-α, TNF-α + scramble, TNF-α + miR-4262 mimic, TNF-α + NC, and TNF-α + miR-4262 inhibitor groups using CCK-8; (F) The cell apoptosis in control, TNF-α, TNF-α + scramble, TNF-α + miR-4262 mimic, TNF-α + NC, and TNF-α + miR-4262 inhibitor groups using TUNEL staining; (G) The expression of autophagy-related proteins, including ULK1, ALG5, Beclin-1, LC3II/LC3I, in control, TNF-α, TNF-α+E64d+pepstatin (A) TNF-α + scramble, TNF-α + miR-4262 mimic, TNF-α + NC, and TNF-α + miR-4262 inhibitor groups using western blotting; (H) The expression of matrix synthesis-related proteins, such as COL2A1, ACAN, MMP-13 and ADAMTS-5, in control, TNF-α, TNF-α + scramble, TNF-α + miR-4262 mimic, TNF-α + NC, and TNF-α + miR-4262 inhibitor groups using western blotting. Three independent experiments were performed in each assay. *P<0.05, **P<0.01, and ***P<0.001 TNF-α, tumor necrosis factor-α; ULK1, uncoordinated 51-like kinase 1; ALG5, asparagine-linked glycosylation 5; COL2A1, type II collagen; ACAN, aggrecan; MMP-13, matrix metallo protease 13; ADAMTS-5, a disintegrin and metalloproteinase with thrombospondin motifs-5.

Article Snippet: Total 50 µg protein sample (per lane) was separated on SDS-PAGE gel, blotted onto PVDF membranes, and blocked in 5% non-fat milk for 1 h. The membranes were probed with mouse polyclonal antibodies to ULK1 (120 kDa; 1;1,000; ab128859; Abcam, Cambridge, UK), ALG5 (32 kDa; 1;1,000; ab108327; Abcam), Beclin-1 (52 kDa; 1;1,000; ab62557; Abcam), LC3II/LC3I (LC3-II, 17 kDa, LC3-II 19 kDa; 1;1,000; ab48394; Abcam), COL2A1 (142 kDa; 1;1,000; ab34712; Abcam), ACAN (250 kDa; 1;1,000; ab36861; Abcam), MMP-13 (54 kDa; 1;1,000; ab39012; Abcam), ADAMTS-5 (73 kDa; 1;1,000; ab41037; Abcam), SIRT1 (120 kDa; 1;1,000; ab110304; Abcam), phospho-PI3K (p-PI3K) (84 kDa; 1;1,000; ab182651; Abcam), PI3K (123 kDa; 1;1,000; ab151549; Abcam), p-AKT (65 kDa; 1;1,000; SAB4301414; Sigma-Aldrich; Merck KGaA), AKT (55 kDa; 1;1,000; SAB4500797; Sigma-Aldrich; Merck KGaA), p-mTOR (250 kDa; 1;1,000; ab137133; Abcam), mTOR (252 kDa; 1;2,000; ab2732; Abcam), and GAPDH (36 kDa; 1;2,000; ab8245; Abcam) overnight at 4°C, respectively.

Techniques: CCK-8 Assay, TUNEL Assay, Staining, Expressing, Western Blot

Upregulated SIRT1 increases cell viability, autophagy, and matrix synthesis as well as decreases apoptosis in TNF-α-treated chondrocytes. (A) The SIRT1 level in control, pEX, pEX-SIRT1, siNC, and si-SIRT1 groups by qPCR; (B) The SIRT1 level in control, pEX, pEX-SIRT1, siNC, and si-SIRT1 groups by western blotting; The cell viability in (C) control, TNF-α, TNF-α + pEX, TNF-α + pEX-SIRT1, TNF-α + siNC, and TNF-α + si-SIRT1 groups using CCK-8; (D) The cell apoptosis in control, TNF-α, TNF-α + pEX, TNF-α + pEX-SIRT1, TNF-α + siNC, and TNF-α + si-SIRT1 groups using TUNEL staining; (E) The expression of autophagy-related proteins, including ULK1, ALG5, Beclin-1, LC3II/LC3I, in control, TNF-α, TNF-α + pEX, TNF-α + pEX-SIRT1, TNF-α + siNC, and TNF-α + si-SIRT1 groups using qPCR; (F) The expression of matrix synthesis-related proteins, such as COL2A1, ACAN, MMP-13 and ADAMTS-5, in control, TNF-α, TNF-α + pEX, TNF-α + pEX-SIRT1, TNF-α + siNC, and TNF-α + si-SIRT1 groups using qPCR. Three independent experiments were performed in each assay. *P<0.05, and **P<0.01 TNF-α, tumor necrosis factor-α; ULK1, uncoordinated 51-like kinase 1; ALG5, asparagine-linked glycosylation 5; COL2A1, type II collagen; ACAN, aggrecan; MMP-13, matrix metallo protease 13; ADAMTS-5, a disintegrin and metalloproteinase with thrombospondin motifs-5; SIRT1, sirtuin type 1.

Journal: Experimental and Therapeutic Medicine

Article Title: miR-4262 regulates chondrocyte viability, apoptosis, autophagy by targeting SIRT1 and activating PI3K/AKT/mTOR signaling pathway in rats with osteoarthritis

doi: 10.3892/etm.2017.5444

Figure Lengend Snippet: Upregulated SIRT1 increases cell viability, autophagy, and matrix synthesis as well as decreases apoptosis in TNF-α-treated chondrocytes. (A) The SIRT1 level in control, pEX, pEX-SIRT1, siNC, and si-SIRT1 groups by qPCR; (B) The SIRT1 level in control, pEX, pEX-SIRT1, siNC, and si-SIRT1 groups by western blotting; The cell viability in (C) control, TNF-α, TNF-α + pEX, TNF-α + pEX-SIRT1, TNF-α + siNC, and TNF-α + si-SIRT1 groups using CCK-8; (D) The cell apoptosis in control, TNF-α, TNF-α + pEX, TNF-α + pEX-SIRT1, TNF-α + siNC, and TNF-α + si-SIRT1 groups using TUNEL staining; (E) The expression of autophagy-related proteins, including ULK1, ALG5, Beclin-1, LC3II/LC3I, in control, TNF-α, TNF-α + pEX, TNF-α + pEX-SIRT1, TNF-α + siNC, and TNF-α + si-SIRT1 groups using qPCR; (F) The expression of matrix synthesis-related proteins, such as COL2A1, ACAN, MMP-13 and ADAMTS-5, in control, TNF-α, TNF-α + pEX, TNF-α + pEX-SIRT1, TNF-α + siNC, and TNF-α + si-SIRT1 groups using qPCR. Three independent experiments were performed in each assay. *P<0.05, and **P<0.01 TNF-α, tumor necrosis factor-α; ULK1, uncoordinated 51-like kinase 1; ALG5, asparagine-linked glycosylation 5; COL2A1, type II collagen; ACAN, aggrecan; MMP-13, matrix metallo protease 13; ADAMTS-5, a disintegrin and metalloproteinase with thrombospondin motifs-5; SIRT1, sirtuin type 1.

Article Snippet: Total 50 µg protein sample (per lane) was separated on SDS-PAGE gel, blotted onto PVDF membranes, and blocked in 5% non-fat milk for 1 h. The membranes were probed with mouse polyclonal antibodies to ULK1 (120 kDa; 1;1,000; ab128859; Abcam, Cambridge, UK), ALG5 (32 kDa; 1;1,000; ab108327; Abcam), Beclin-1 (52 kDa; 1;1,000; ab62557; Abcam), LC3II/LC3I (LC3-II, 17 kDa, LC3-II 19 kDa; 1;1,000; ab48394; Abcam), COL2A1 (142 kDa; 1;1,000; ab34712; Abcam), ACAN (250 kDa; 1;1,000; ab36861; Abcam), MMP-13 (54 kDa; 1;1,000; ab39012; Abcam), ADAMTS-5 (73 kDa; 1;1,000; ab41037; Abcam), SIRT1 (120 kDa; 1;1,000; ab110304; Abcam), phospho-PI3K (p-PI3K) (84 kDa; 1;1,000; ab182651; Abcam), PI3K (123 kDa; 1;1,000; ab151549; Abcam), p-AKT (65 kDa; 1;1,000; SAB4301414; Sigma-Aldrich; Merck KGaA), AKT (55 kDa; 1;1,000; SAB4500797; Sigma-Aldrich; Merck KGaA), p-mTOR (250 kDa; 1;1,000; ab137133; Abcam), mTOR (252 kDa; 1;2,000; ab2732; Abcam), and GAPDH (36 kDa; 1;2,000; ab8245; Abcam) overnight at 4°C, respectively.

Techniques: Western Blot, CCK-8 Assay, TUNEL Assay, Staining, Expressing

Effects of miR-4262 on cell viability, cell apoptosis, cell autophagy, and matrix synthesis is inhibited by SIRT1. (A) The cell viability in control, TNF-α, TNF-α + scramble + pEX, TNF-α + miR-4262 mimic, and TNF-α + miR-4262 mimic + pEX-SIRT1 groups using CCK-8; (B) The cell apoptosis in control, TNF-α, TNF-α + scramble + pEX, TNF-α + miR-4262 mimic, and TNF-α + miR-4262 mimic + pEX-SIRT1 groups using TUNEL staining; (C) The expression of autophagy-related proteins, including ULK1, ALG5, Beclin-1, LC3II/LC3I, in control, TNF-α, TNF-α + scramble + pEX, TNF-α + miR-4262 mimic, and TNF-α + miR-4262 mimic + pEX-SIRT1 groups using western blotting; (D) The expression of matrix synthesis-related proteins, such as COL2A1, ACAN, MMP-13 and ADAMTS-5, in control, TNF-α, TNF-α + scramble + pEX, TNF-α + miR-4262 mimic, and TNF-α + miR-4262 mimic + pEX-SIRT1 groups using western blotting. Three independent experiments were performed in each assay. *P<0.05, and **P<0.01 TNF-α, tumor necrosis factor-α; ULK1, uncoordinated 51-like kinase 1; ALG5, asparagine-linked glycosylation 5; COL2A1, type II collagen; ACAN, aggrecan; MMP-13, matrix metallo protease 13; ADAMTS-5, a disintegrin and metalloproteinase with thrombospondin motifs-5; SIRT1, sirtuin type 1.

Journal: Experimental and Therapeutic Medicine

Article Title: miR-4262 regulates chondrocyte viability, apoptosis, autophagy by targeting SIRT1 and activating PI3K/AKT/mTOR signaling pathway in rats with osteoarthritis

doi: 10.3892/etm.2017.5444

Figure Lengend Snippet: Effects of miR-4262 on cell viability, cell apoptosis, cell autophagy, and matrix synthesis is inhibited by SIRT1. (A) The cell viability in control, TNF-α, TNF-α + scramble + pEX, TNF-α + miR-4262 mimic, and TNF-α + miR-4262 mimic + pEX-SIRT1 groups using CCK-8; (B) The cell apoptosis in control, TNF-α, TNF-α + scramble + pEX, TNF-α + miR-4262 mimic, and TNF-α + miR-4262 mimic + pEX-SIRT1 groups using TUNEL staining; (C) The expression of autophagy-related proteins, including ULK1, ALG5, Beclin-1, LC3II/LC3I, in control, TNF-α, TNF-α + scramble + pEX, TNF-α + miR-4262 mimic, and TNF-α + miR-4262 mimic + pEX-SIRT1 groups using western blotting; (D) The expression of matrix synthesis-related proteins, such as COL2A1, ACAN, MMP-13 and ADAMTS-5, in control, TNF-α, TNF-α + scramble + pEX, TNF-α + miR-4262 mimic, and TNF-α + miR-4262 mimic + pEX-SIRT1 groups using western blotting. Three independent experiments were performed in each assay. *P<0.05, and **P<0.01 TNF-α, tumor necrosis factor-α; ULK1, uncoordinated 51-like kinase 1; ALG5, asparagine-linked glycosylation 5; COL2A1, type II collagen; ACAN, aggrecan; MMP-13, matrix metallo protease 13; ADAMTS-5, a disintegrin and metalloproteinase with thrombospondin motifs-5; SIRT1, sirtuin type 1.

Article Snippet: Total 50 µg protein sample (per lane) was separated on SDS-PAGE gel, blotted onto PVDF membranes, and blocked in 5% non-fat milk for 1 h. The membranes were probed with mouse polyclonal antibodies to ULK1 (120 kDa; 1;1,000; ab128859; Abcam, Cambridge, UK), ALG5 (32 kDa; 1;1,000; ab108327; Abcam), Beclin-1 (52 kDa; 1;1,000; ab62557; Abcam), LC3II/LC3I (LC3-II, 17 kDa, LC3-II 19 kDa; 1;1,000; ab48394; Abcam), COL2A1 (142 kDa; 1;1,000; ab34712; Abcam), ACAN (250 kDa; 1;1,000; ab36861; Abcam), MMP-13 (54 kDa; 1;1,000; ab39012; Abcam), ADAMTS-5 (73 kDa; 1;1,000; ab41037; Abcam), SIRT1 (120 kDa; 1;1,000; ab110304; Abcam), phospho-PI3K (p-PI3K) (84 kDa; 1;1,000; ab182651; Abcam), PI3K (123 kDa; 1;1,000; ab151549; Abcam), p-AKT (65 kDa; 1;1,000; SAB4301414; Sigma-Aldrich; Merck KGaA), AKT (55 kDa; 1;1,000; SAB4500797; Sigma-Aldrich; Merck KGaA), p-mTOR (250 kDa; 1;1,000; ab137133; Abcam), mTOR (252 kDa; 1;2,000; ab2732; Abcam), and GAPDH (36 kDa; 1;2,000; ab8245; Abcam) overnight at 4°C, respectively.

Techniques: CCK-8 Assay, TUNEL Assay, Staining, Expressing, Western Blot