hif 1α Search Results


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Santa Cruz Biotechnology polyclonal human mouse anti hif 1α antibody
Fig. 6. Gene expression of <t>HIF-1α</t> under BEC in differentiation condition. Rat calvarial osteoblasts were exposed to BEC (1.5 μA/cm2, 3000 Hz) for 4 days in interrupted (6 h/day) and continuous (24 h/day) mode under differentiation conditions. HIF-1α mRNA expression was determined by RT-PCR (A) and real- time RT-PCR (B) (mean±SEM, n=3). Difference from control was not significant as p>0.05. (C) HIF-1α protein level was determined by western blotting. Results shown are representative of two independent experiments.
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Santa Cruz Biotechnology hif 1α sirna
Fig. 6. Gene expression of <t>HIF-1α</t> under BEC in differentiation condition. Rat calvarial osteoblasts were exposed to BEC (1.5 μA/cm2, 3000 Hz) for 4 days in interrupted (6 h/day) and continuous (24 h/day) mode under differentiation conditions. HIF-1α mRNA expression was determined by RT-PCR (A) and real- time RT-PCR (B) (mean±SEM, n=3). Difference from control was not significant as p>0.05. (C) HIF-1α protein level was determined by western blotting. Results shown are representative of two independent experiments.
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Elabscience Biotechnology rat hif 1α elisa kit
Fig. 6. Gene expression of <t>HIF-1α</t> under BEC in differentiation condition. Rat calvarial osteoblasts were exposed to BEC (1.5 μA/cm2, 3000 Hz) for 4 days in interrupted (6 h/day) and continuous (24 h/day) mode under differentiation conditions. HIF-1α mRNA expression was determined by RT-PCR (A) and real- time RT-PCR (B) (mean±SEM, n=3). Difference from control was not significant as p>0.05. (C) HIF-1α protein level was determined by western blotting. Results shown are representative of two independent experiments.
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Proteintech immunofluorescence
Fig. 6. Gene expression of <t>HIF-1α</t> under BEC in differentiation condition. Rat calvarial osteoblasts were exposed to BEC (1.5 μA/cm2, 3000 Hz) for 4 days in interrupted (6 h/day) and continuous (24 h/day) mode under differentiation conditions. HIF-1α mRNA expression was determined by RT-PCR (A) and real- time RT-PCR (B) (mean±SEM, n=3). Difference from control was not significant as p>0.05. (C) HIF-1α protein level was determined by western blotting. Results shown are representative of two independent experiments.
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Proteintech hif1α proteintech rabbit ab
Fig. 6. Gene expression of <t>HIF-1α</t> under BEC in differentiation condition. Rat calvarial osteoblasts were exposed to BEC (1.5 μA/cm2, 3000 Hz) for 4 days in interrupted (6 h/day) and continuous (24 h/day) mode under differentiation conditions. HIF-1α mRNA expression was determined by RT-PCR (A) and real- time RT-PCR (B) (mean±SEM, n=3). Difference from control was not significant as p>0.05. (C) HIF-1α protein level was determined by western blotting. Results shown are representative of two independent experiments.
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Thermo Fisher hif 1α rs11549465 polymorphism
Association of HIF1α <t>rs11549465</t> genotypes with (A) age, (B) duration of HIV infection, and (C) duration of ART exposure in PLWH with and without MS. * denotes statistical significance ( p <0.05).
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Association of HIF1α <t>rs11549465</t> genotypes with (A) age, (B) duration of HIV infection, and (C) duration of ART exposure in PLWH with and without MS. * denotes statistical significance ( p <0.05).
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Association of HIF1α <t>rs11549465</t> genotypes with (A) age, (B) duration of HIV infection, and (C) duration of ART exposure in PLWH with and without MS. * denotes statistical significance ( p <0.05).
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Santa Cruz Biotechnology mutant dna sequence
Effects of hypoxia or CoCl 2 treatment <t>on</t> <t>HIF-1</t> <t>DNA</t> binding and reporter gene activity in astrocytes. ( A ) Mouse HIF-1α +/+ and HIF-1α +/- cells were exposed to hypoxia or 125 μM CoCl 2 for 6 h, nuclear extracts were then prepared and EMSA carried out as described in the Materials and Methods. HIF-1 in the nuclear extracts isolated from hypoxia or CoCl 2 -treated cells bound to the wild-type probe (lanes #1–6) but not to the mutant probe (lanes #7–12). HIF-1/DNA complex was detected in hypoxia (H)-or CoCl 2 (Co)-treated cells (lanes #2, 3, 5, 6) but not in control (C) cells (lanes #1, 4). More complex (darker band) was seen in hypoxia-or CoCl 2 -treated HIF-1α +/+ cells (lanes #2, 3) than that in hypoxia-or CoCl 2 -treated HIF-1α +/- cells (lanes #5, 6). Supershift assay showed that the HIF-1/DNA complex was shifted up in the presence of wild-type (wt) oligo probe and 4 μg HIF-1α antiboby (lanes #13 & 14). ( B ) The activity of the reporter gene, luciferase yellow, under a wild-type HIF-1-binding sequence from MCP-1 promoter (pGL3/MCP1w) or a mutated sequence (pGL3/MCP1m), was carried out to test the transcriptional activation of MCP-1 by HIF-1 activated by hypoxia. FHAs were transfected with an empty vector, pGL3/MCP1w or pGL3/MCP1m, respectively, and recovered overnight for 16 h. The cells were exposed to normoxia or hypoxia for 4 h and then harvested for luciferase yellow assays. Hypoxia strongly stimulated the reporter gene activity from pGL3/MCP1w but not from the empty vector and pGL3/MCP1m. Each bar represents the mean ± SD of three assays and each assay had at least two replicates. Asterisks indicate significant difference compared to relevant controls (p < 0.05, one-way ANOVA, followed by multiple comparisons among means).
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Cusabio hif1α elisa kit
Effects of hypoxia or CoCl 2 treatment <t>on</t> <t>HIF-1</t> <t>DNA</t> binding and reporter gene activity in astrocytes. ( A ) Mouse HIF-1α +/+ and HIF-1α +/- cells were exposed to hypoxia or 125 μM CoCl 2 for 6 h, nuclear extracts were then prepared and EMSA carried out as described in the Materials and Methods. HIF-1 in the nuclear extracts isolated from hypoxia or CoCl 2 -treated cells bound to the wild-type probe (lanes #1–6) but not to the mutant probe (lanes #7–12). HIF-1/DNA complex was detected in hypoxia (H)-or CoCl 2 (Co)-treated cells (lanes #2, 3, 5, 6) but not in control (C) cells (lanes #1, 4). More complex (darker band) was seen in hypoxia-or CoCl 2 -treated HIF-1α +/+ cells (lanes #2, 3) than that in hypoxia-or CoCl 2 -treated HIF-1α +/- cells (lanes #5, 6). Supershift assay showed that the HIF-1/DNA complex was shifted up in the presence of wild-type (wt) oligo probe and 4 μg HIF-1α antiboby (lanes #13 & 14). ( B ) The activity of the reporter gene, luciferase yellow, under a wild-type HIF-1-binding sequence from MCP-1 promoter (pGL3/MCP1w) or a mutated sequence (pGL3/MCP1m), was carried out to test the transcriptional activation of MCP-1 by HIF-1 activated by hypoxia. FHAs were transfected with an empty vector, pGL3/MCP1w or pGL3/MCP1m, respectively, and recovered overnight for 16 h. The cells were exposed to normoxia or hypoxia for 4 h and then harvested for luciferase yellow assays. Hypoxia strongly stimulated the reporter gene activity from pGL3/MCP1w but not from the empty vector and pGL3/MCP1m. Each bar represents the mean ± SD of three assays and each assay had at least two replicates. Asterisks indicate significant difference compared to relevant controls (p < 0.05, one-way ANOVA, followed by multiple comparisons among means).
Hif1α Elisa Kit, supplied by Cusabio, 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


Fig. 6. Gene expression of HIF-1α under BEC in differentiation condition. Rat calvarial osteoblasts were exposed to BEC (1.5 μA/cm2, 3000 Hz) for 4 days in interrupted (6 h/day) and continuous (24 h/day) mode under differentiation conditions. HIF-1α mRNA expression was determined by RT-PCR (A) and real- time RT-PCR (B) (mean±SEM, n=3). Difference from control was not significant as p>0.05. (C) HIF-1α protein level was determined by western blotting. Results shown are representative of two independent experiments.

Journal: Biochimica et biophysica acta

Article Title: Biphasic electric current stimulates proliferation and induces VEGF production in osteoblasts.

doi: 10.1016/j.bbamcr.2006.06.007

Figure Lengend Snippet: Fig. 6. Gene expression of HIF-1α under BEC in differentiation condition. Rat calvarial osteoblasts were exposed to BEC (1.5 μA/cm2, 3000 Hz) for 4 days in interrupted (6 h/day) and continuous (24 h/day) mode under differentiation conditions. HIF-1α mRNA expression was determined by RT-PCR (A) and real- time RT-PCR (B) (mean±SEM, n=3). Difference from control was not significant as p>0.05. (C) HIF-1α protein level was determined by western blotting. Results shown are representative of two independent experiments.

Article Snippet: The following antibodies were used in this study: polyclonal human/mouse anti-HIF-1α antibody diluted 1:100 with (AB1536, R&D systems, USA), monoclonal anti-αtubulin (Santa Cruz Biotechnology, Inc. USA).

Techniques: Gene Expression, Expressing, Reverse Transcription Polymerase Chain Reaction, Quantitative RT-PCR, Control, Western Blot

Association of HIF1α rs11549465 genotypes with (A) age, (B) duration of HIV infection, and (C) duration of ART exposure in PLWH with and without MS. * denotes statistical significance ( p <0.05).

Journal: Frontiers in Medicine

Article Title: Protective association of the HIF-1α rs11549465 polymorphism with metabolic syndrome in people living with HIV on antiretroviral therapy

doi: 10.3389/fmed.2026.1802450

Figure Lengend Snippet: Association of HIF1α rs11549465 genotypes with (A) age, (B) duration of HIV infection, and (C) duration of ART exposure in PLWH with and without MS. * denotes statistical significance ( p <0.05).

Article Snippet: Genotyping of the HIF-1α rs11549465 polymorphism was performed by real-time PCR using a TaqMan SNP Genotyping Assay (C__25473074_10) on an ABI 7500 Real-time System (Applied Biosystems, Foster, California, USA).

Techniques: Infection

Exploratory stratified analysis of the association between the HIF1α rs11549465 CT genotype and prevalent MS according to duration of (A) HIV infection and (B) ART exposure. Odds ratios (ORs) represent unadjusted estimates comparing CT genotype carriers to non-CT genotypes (reference group) within each duration category. Vertical lines indicate 95% confidence intervals (log scale). Sample sizes for MS and control groups are indicated for each stratum. (A) Stratified by duration of HIV infection. In the 0–10-years category, the frequency of the CT genotype was 11.8% (2/17) in MS group and 47.7% (21/44) in the control group (OR = 0.15; 95% CI 0.03–0.72, p = 0.017). In the 11–20-years category CT genotype frequency was 30% (6/20) in the MS group and 56% (14/25) in controls (OR = 0.34; 95% CI 0.10–1.16, p = 0.131). In the > 20-years category, CT genotype frequencies were 60% (6/10) in the MS group compared to 60% (3/5) in controls (OR = 1.00, 95% CI 0.11–8.95, p = 1.000). (B) Stratified by duration of ART exposure. In the 0–10-years ART duration category, the frequency of CT genotype was 11.1% (2/18) in MS group and 47.8% (22/46) in the control group (OR = 0.14; 95% CI 0.03–0.66, p = 0.009). In the 11–20-years category, CT genotype frequencies were 31.6% (6/19) in the MS group and 58% (14/24) in controls (OR = 0.33, 95% CI 0.09–1.17, p = 0.125). In the >20 years ART duration category, CT genotype frequencies were 60% (6/10) in MS compared to 50% (2/4) in controls (OR = 1.50; 95% CI 0.15–15.46, p = 1.000).

Journal: Frontiers in Medicine

Article Title: Protective association of the HIF-1α rs11549465 polymorphism with metabolic syndrome in people living with HIV on antiretroviral therapy

doi: 10.3389/fmed.2026.1802450

Figure Lengend Snippet: Exploratory stratified analysis of the association between the HIF1α rs11549465 CT genotype and prevalent MS according to duration of (A) HIV infection and (B) ART exposure. Odds ratios (ORs) represent unadjusted estimates comparing CT genotype carriers to non-CT genotypes (reference group) within each duration category. Vertical lines indicate 95% confidence intervals (log scale). Sample sizes for MS and control groups are indicated for each stratum. (A) Stratified by duration of HIV infection. In the 0–10-years category, the frequency of the CT genotype was 11.8% (2/17) in MS group and 47.7% (21/44) in the control group (OR = 0.15; 95% CI 0.03–0.72, p = 0.017). In the 11–20-years category CT genotype frequency was 30% (6/20) in the MS group and 56% (14/25) in controls (OR = 0.34; 95% CI 0.10–1.16, p = 0.131). In the > 20-years category, CT genotype frequencies were 60% (6/10) in the MS group compared to 60% (3/5) in controls (OR = 1.00, 95% CI 0.11–8.95, p = 1.000). (B) Stratified by duration of ART exposure. In the 0–10-years ART duration category, the frequency of CT genotype was 11.1% (2/18) in MS group and 47.8% (22/46) in the control group (OR = 0.14; 95% CI 0.03–0.66, p = 0.009). In the 11–20-years category, CT genotype frequencies were 31.6% (6/19) in the MS group and 58% (14/24) in controls (OR = 0.33, 95% CI 0.09–1.17, p = 0.125). In the >20 years ART duration category, CT genotype frequencies were 60% (6/10) in MS compared to 50% (2/4) in controls (OR = 1.50; 95% CI 0.15–15.46, p = 1.000).

Article Snippet: Genotyping of the HIF-1α rs11549465 polymorphism was performed by real-time PCR using a TaqMan SNP Genotyping Assay (C__25473074_10) on an ABI 7500 Real-time System (Applied Biosystems, Foster, California, USA).

Techniques: Infection, Control

Effects of hypoxia or CoCl 2 treatment on HIF-1 DNA binding and reporter gene activity in astrocytes. ( A ) Mouse HIF-1α +/+ and HIF-1α +/- cells were exposed to hypoxia or 125 μM CoCl 2 for 6 h, nuclear extracts were then prepared and EMSA carried out as described in the Materials and Methods. HIF-1 in the nuclear extracts isolated from hypoxia or CoCl 2 -treated cells bound to the wild-type probe (lanes #1–6) but not to the mutant probe (lanes #7–12). HIF-1/DNA complex was detected in hypoxia (H)-or CoCl 2 (Co)-treated cells (lanes #2, 3, 5, 6) but not in control (C) cells (lanes #1, 4). More complex (darker band) was seen in hypoxia-or CoCl 2 -treated HIF-1α +/+ cells (lanes #2, 3) than that in hypoxia-or CoCl 2 -treated HIF-1α +/- cells (lanes #5, 6). Supershift assay showed that the HIF-1/DNA complex was shifted up in the presence of wild-type (wt) oligo probe and 4 μg HIF-1α antiboby (lanes #13 & 14). ( B ) The activity of the reporter gene, luciferase yellow, under a wild-type HIF-1-binding sequence from MCP-1 promoter (pGL3/MCP1w) or a mutated sequence (pGL3/MCP1m), was carried out to test the transcriptional activation of MCP-1 by HIF-1 activated by hypoxia. FHAs were transfected with an empty vector, pGL3/MCP1w or pGL3/MCP1m, respectively, and recovered overnight for 16 h. The cells were exposed to normoxia or hypoxia for 4 h and then harvested for luciferase yellow assays. Hypoxia strongly stimulated the reporter gene activity from pGL3/MCP1w but not from the empty vector and pGL3/MCP1m. Each bar represents the mean ± SD of three assays and each assay had at least two replicates. Asterisks indicate significant difference compared to relevant controls (p < 0.05, one-way ANOVA, followed by multiple comparisons among means).

Journal: Journal of Neuroinflammation

Article Title: Hypoxia-inducible factor-1 (HIF-1) is involved in the regulation of hypoxia-stimulated expression of monocyte chemoattractant protein-1 (MCP-1/CCL2) and MCP-5 (Ccl12) in astrocytes

doi: 10.1186/1742-2094-4-12

Figure Lengend Snippet: Effects of hypoxia or CoCl 2 treatment on HIF-1 DNA binding and reporter gene activity in astrocytes. ( A ) Mouse HIF-1α +/+ and HIF-1α +/- cells were exposed to hypoxia or 125 μM CoCl 2 for 6 h, nuclear extracts were then prepared and EMSA carried out as described in the Materials and Methods. HIF-1 in the nuclear extracts isolated from hypoxia or CoCl 2 -treated cells bound to the wild-type probe (lanes #1–6) but not to the mutant probe (lanes #7–12). HIF-1/DNA complex was detected in hypoxia (H)-or CoCl 2 (Co)-treated cells (lanes #2, 3, 5, 6) but not in control (C) cells (lanes #1, 4). More complex (darker band) was seen in hypoxia-or CoCl 2 -treated HIF-1α +/+ cells (lanes #2, 3) than that in hypoxia-or CoCl 2 -treated HIF-1α +/- cells (lanes #5, 6). Supershift assay showed that the HIF-1/DNA complex was shifted up in the presence of wild-type (wt) oligo probe and 4 μg HIF-1α antiboby (lanes #13 & 14). ( B ) The activity of the reporter gene, luciferase yellow, under a wild-type HIF-1-binding sequence from MCP-1 promoter (pGL3/MCP1w) or a mutated sequence (pGL3/MCP1m), was carried out to test the transcriptional activation of MCP-1 by HIF-1 activated by hypoxia. FHAs were transfected with an empty vector, pGL3/MCP1w or pGL3/MCP1m, respectively, and recovered overnight for 16 h. The cells were exposed to normoxia or hypoxia for 4 h and then harvested for luciferase yellow assays. Hypoxia strongly stimulated the reporter gene activity from pGL3/MCP1w but not from the empty vector and pGL3/MCP1m. Each bar represents the mean ± SD of three assays and each assay had at least two replicates. Asterisks indicate significant difference compared to relevant controls (p < 0.05, one-way ANOVA, followed by multiple comparisons among means).

Article Snippet: For the EMSA, a typical double-stranded consensus oligonucleotide for HIF-1 binding (5'-TCTGT ACGTG ACCACACTCACCTC-3') and a mutant DNA sequence (5'-TCTGT AAAAG ACCACACTCACCTC-3') [ , ] were purchased from Santa Cruz Biotech Inc (CAT # sc-2625, Santa Cruz, CA) and end-labeled with γ[ 32 P]-ATP (Mandel/NEN Life Science, Guelph, ON).

Techniques: Binding Assay, Activity Assay, Isolation, Mutagenesis, Control, Luciferase, Sequencing, Activation Assay, Transfection, Plasmid Preparation