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rnase inhibitor  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology rnase inhibitor
    Rnase Inhibitor, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 37 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pla+blocking+solution/RNase+Inhibitor/pmc03792345-203-155-66
    Average 93 stars, based on 37 article reviews
    rnase inhibitor - by Bioz Stars, 2026-11
    93/100 stars

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    Related Articles

    Lysis:

    Article Title: Androgen-targeted hsa_circ_0085121 encodes a novel protein and improves the development of prostate cancer through facilitating the activity of PI3K/Akt/mTOR pathway and enhancing AR-V7 alternative splicing
    Article Snippet: .. Nuclear extracts were solubilized in RIP lysis buffer [100 mM KCl, 5 mM MgCl2, 10 mM HEPES (pH 7.4), 0.5% Nonidet P-40, 1 mM DTT, protease and phosphatase inhibitor mixtures, 100 U/mL RNase OUT] and precleared with 5 μg of control IgG and Protein A/G agarose beads (Santa Cruz Biotechnology). ..

    Control:

    Article Title: Androgen-targeted hsa_circ_0085121 encodes a novel protein and improves the development of prostate cancer through facilitating the activity of PI3K/Akt/mTOR pathway and enhancing AR-V7 alternative splicing
    Article Snippet: .. Nuclear extracts were solubilized in RIP lysis buffer [100 mM KCl, 5 mM MgCl2, 10 mM HEPES (pH 7.4), 0.5% Nonidet P-40, 1 mM DTT, protease and phosphatase inhibitor mixtures, 100 U/mL RNase OUT] and precleared with 5 μg of control IgG and Protein A/G agarose beads (Santa Cruz Biotechnology). ..

    Protease Inhibitor:

    Article Title: Fructose-1,6-diphosphate inhibits viral replication by promoting the lysosomal degradation of HMGB1 and blocking the binding of HMGB1 to the viral genome.
    Article Snippet: .. The cells were pelleted and washed with 500 μL PBS, and then the cells were lysed with RIPA buffer PLOS Pathogens | https://doi.org/10.1371/journal.ppat.1012782 December 18, 2024 19 / 26 supplemented with a protease inhibitor cocktail and an RNase inhibitor on ice for 30 min. Immunoprecipitation was performed using antibodies against HMGB1 (sc-56698, Santa Cruz Biotechnology). ..

    Article Title: Fructose-1,6-diphosphate inhibits viral replication by promoting the lysosomal degradation of HMGB1 and blocking the binding of HMGB1 to the viral genome
    Article Snippet: .. The cells were pelleted and washed with 500 μL PBS, and then the cells were lysed with RIPA buffer supplemented with a protease inhibitor cocktail and an RNase inhibitor on ice for 30 min. Immunoprecipitation was performed using antibodies against HMGB1 (sc-56698, Santa Cruz Biotechnology). ..

    Immunoprecipitation:

    Article Title: Fructose-1,6-diphosphate inhibits viral replication by promoting the lysosomal degradation of HMGB1 and blocking the binding of HMGB1 to the viral genome.
    Article Snippet: .. The cells were pelleted and washed with 500 μL PBS, and then the cells were lysed with RIPA buffer PLOS Pathogens | https://doi.org/10.1371/journal.ppat.1012782 December 18, 2024 19 / 26 supplemented with a protease inhibitor cocktail and an RNase inhibitor on ice for 30 min. Immunoprecipitation was performed using antibodies against HMGB1 (sc-56698, Santa Cruz Biotechnology). ..

    Article Title: Fructose-1,6-diphosphate inhibits viral replication by promoting the lysosomal degradation of HMGB1 and blocking the binding of HMGB1 to the viral genome
    Article Snippet: .. The cells were pelleted and washed with 500 μL PBS, and then the cells were lysed with RIPA buffer supplemented with a protease inhibitor cocktail and an RNase inhibitor on ice for 30 min. Immunoprecipitation was performed using antibodies against HMGB1 (sc-56698, Santa Cruz Biotechnology). ..

    Incubation:

    Article Title: miR-340-3p-modified bone marrow mesenchymal stem cell-derived exosomes inhibit ferroptosis through METTL3-mediated m 6 A modification of HMOX1 to promote recovery of injured rat uterus.
    Article Snippet: .. Furthermore, we incubated the supernatant with anti-YTHDF2 Abs in 1 × IP buffer (500 μL) containing RNase inhibitors or Protein A/G Plus agarose (Santa Cruz Biotechnology, sc-2003) overnight at 4°C following RNase T1 (1 U; Thermo Fisher Scientific, EN0541) treatment for 15 min at 24 °C. ..

    Article Title: CircHAT1 regulates the proliferation and phenotype switch of vascular smooth muscle cells in lower extremity arteriosclerosis obliterans through targeting SFRS1.
    Article Snippet: This study aimed to decipher the mechanism of circular ribonucleic acids (circRNAs) in lower extremity arteriosclerosis obliterans (LEASO).. First, bioinformatics analysis was performed for screening significantly down-regulated cardiac specific circRNA—circHAT1 in LEASO.. The expression of circHAT1 in LEASO clinical samples was detected by quantitative real-time polymerase chain reaction (qRT-PCR).

    Article Title: Magnesium ions facilitate osteogenic differentiation and intervertebral fusion via m6A methylation of RhoA mRNA
    Article Snippet: Total RNA was extracted from cells using TRIzol reagent and quantified with a NanoDrop microspectrophotometer. .. 600 μg of total RNA was mixed with 12 μg of anti-m6A antibody (ab151230, Abcam) in IP buffer (10 mmol/L pH 7.4 Tris-HCl, 150 mmol/L NaCl, 0.1% NP-40, and 40 U/μL RNAse inhibitor) and incubated at 4 °C with rotation for 2 h. To block, 15 μL of protein A (LSKMAGA10, Millipore) and 15 μL of protein G (LSKMAGG10, Millipore) magnetic beads were added to the IP buffer containing BSA (0.5 mg/mL) and incubated at 4 °C with rotation for 2 h. The IP mixture and blocked magnetic beads were then combined and incubated at 4 °C with rotation for 2 h. The mixture was eluted with m6A 5′-monophosphate sodium salt (6.7 mmol/L, sc-215524, Santa Cruz) dissolved in IP buffer, and the eluates were combined. ..

    Blocking Assay:

    Article Title: Magnesium ions facilitate osteogenic differentiation and intervertebral fusion via m6A methylation of RhoA mRNA
    Article Snippet: Total RNA was extracted from cells using TRIzol reagent and quantified with a NanoDrop microspectrophotometer. .. 600 μg of total RNA was mixed with 12 μg of anti-m6A antibody (ab151230, Abcam) in IP buffer (10 mmol/L pH 7.4 Tris-HCl, 150 mmol/L NaCl, 0.1% NP-40, and 40 U/μL RNAse inhibitor) and incubated at 4 °C with rotation for 2 h. To block, 15 μL of protein A (LSKMAGA10, Millipore) and 15 μL of protein G (LSKMAGG10, Millipore) magnetic beads were added to the IP buffer containing BSA (0.5 mg/mL) and incubated at 4 °C with rotation for 2 h. The IP mixture and blocked magnetic beads were then combined and incubated at 4 °C with rotation for 2 h. The mixture was eluted with m6A 5′-monophosphate sodium salt (6.7 mmol/L, sc-215524, Santa Cruz) dissolved in IP buffer, and the eluates were combined. ..

    Magnetic Beads:

    Article Title: Magnesium ions facilitate osteogenic differentiation and intervertebral fusion via m6A methylation of RhoA mRNA
    Article Snippet: Total RNA was extracted from cells using TRIzol reagent and quantified with a NanoDrop microspectrophotometer. .. 600 μg of total RNA was mixed with 12 μg of anti-m6A antibody (ab151230, Abcam) in IP buffer (10 mmol/L pH 7.4 Tris-HCl, 150 mmol/L NaCl, 0.1% NP-40, and 40 U/μL RNAse inhibitor) and incubated at 4 °C with rotation for 2 h. To block, 15 μL of protein A (LSKMAGA10, Millipore) and 15 μL of protein G (LSKMAGG10, Millipore) magnetic beads were added to the IP buffer containing BSA (0.5 mg/mL) and incubated at 4 °C with rotation for 2 h. The IP mixture and blocked magnetic beads were then combined and incubated at 4 °C with rotation for 2 h. The mixture was eluted with m6A 5′-monophosphate sodium salt (6.7 mmol/L, sc-215524, Santa Cruz) dissolved in IP buffer, and the eluates were combined. ..



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    Loss of BTG3 leads to reduced mobility of XPC at damage sites. ( A – C ) Colocalization of BTG3 and XPC at damage sites after UV. <t>PLA</t> was conducted <t>with</t> <t>HaCaT</t> cells using anti-BTG3 and anti-XPC (A). Mean fluorescence intensity and PLA foci number were quantified and shown in panels (B) and (C), respectively, with n ≧ 100. Data were analyzed using unpaired two-tailed t -test and presented as mean ± SEM Scale bar, 10 μm. ( D ) Co-immunoprecipitation of endogenous BTG3 and XPC from HaCaT cells. ( E, F ) Retention of XPC at localized UV damage in BTG3 KO cells. Localized UVC-irradiation (100 J/m 2 ) was performed with 5 μM isopore membrane filter and XPC loading at localized UV damage sites was assessed using confocal microscopy (E). Scale bar, 10 μm. Percent cells with XPC-positive foci were counted and presented as mean ± SEM in panel (F). Data were analyzed using unpaired two-tailed t -test. n ≧ 50. ( G, H ) Mobility of XPC was reduced in BTG3 KO cells. The mobility of XPC-GFP in mock-treated or global UV-irradiated (20 J/m 2 ) parental and BTG3 KO HEK293T cells was assessed using FRAP. Fluorescence recovery was monitored over 120 s and normalized to prebleach intensity ( n = 36 from 3 independent experiments) (G). Data were analyzed using unpaired two-tailed t -tests and shown as mean ± SEM in panel (H).
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    Loss of BTG3 leads to reduced mobility of XPC at damage sites. ( A – C ) Colocalization of BTG3 and XPC at damage sites after UV. <t>PLA</t> was conducted <t>with</t> <t>HaCaT</t> cells using anti-BTG3 and anti-XPC (A). Mean fluorescence intensity and PLA foci number were quantified and shown in panels (B) and (C), respectively, with n ≧ 100. Data were analyzed using unpaired two-tailed t -test and presented as mean ± SEM Scale bar, 10 μm. ( D ) Co-immunoprecipitation of endogenous BTG3 and XPC from HaCaT cells. ( E, F ) Retention of XPC at localized UV damage in BTG3 KO cells. Localized UVC-irradiation (100 J/m 2 ) was performed with 5 μM isopore membrane filter and XPC loading at localized UV damage sites was assessed using confocal microscopy (E). Scale bar, 10 μm. Percent cells with XPC-positive foci were counted and presented as mean ± SEM in panel (F). Data were analyzed using unpaired two-tailed t -test. n ≧ 50. ( G, H ) Mobility of XPC was reduced in BTG3 KO cells. The mobility of XPC-GFP in mock-treated or global UV-irradiated (20 J/m 2 ) parental and BTG3 KO HEK293T cells was assessed using FRAP. Fluorescence recovery was monitored over 120 s and normalized to prebleach intensity ( n = 36 from 3 independent experiments) (G). Data were analyzed using unpaired two-tailed t -tests and shown as mean ± SEM in panel (H).
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    Image Search Results


    Loss of BTG3 leads to reduced mobility of XPC at damage sites. ( A – C ) Colocalization of BTG3 and XPC at damage sites after UV. PLA was conducted with HaCaT cells using anti-BTG3 and anti-XPC (A). Mean fluorescence intensity and PLA foci number were quantified and shown in panels (B) and (C), respectively, with n ≧ 100. Data were analyzed using unpaired two-tailed t -test and presented as mean ± SEM Scale bar, 10 μm. ( D ) Co-immunoprecipitation of endogenous BTG3 and XPC from HaCaT cells. ( E, F ) Retention of XPC at localized UV damage in BTG3 KO cells. Localized UVC-irradiation (100 J/m 2 ) was performed with 5 μM isopore membrane filter and XPC loading at localized UV damage sites was assessed using confocal microscopy (E). Scale bar, 10 μm. Percent cells with XPC-positive foci were counted and presented as mean ± SEM in panel (F). Data were analyzed using unpaired two-tailed t -test. n ≧ 50. ( G, H ) Mobility of XPC was reduced in BTG3 KO cells. The mobility of XPC-GFP in mock-treated or global UV-irradiated (20 J/m 2 ) parental and BTG3 KO HEK293T cells was assessed using FRAP. Fluorescence recovery was monitored over 120 s and normalized to prebleach intensity ( n = 36 from 3 independent experiments) (G). Data were analyzed using unpaired two-tailed t -tests and shown as mean ± SEM in panel (H).

    Journal: Nucleic Acids Research

    Article Title: BTG3-dependent VCP/p97 nuclear translocation is required for efficient repair of UV-induced DNA lesions

    doi: 10.1093/nar/gkaf626

    Figure Lengend Snippet: Loss of BTG3 leads to reduced mobility of XPC at damage sites. ( A – C ) Colocalization of BTG3 and XPC at damage sites after UV. PLA was conducted with HaCaT cells using anti-BTG3 and anti-XPC (A). Mean fluorescence intensity and PLA foci number were quantified and shown in panels (B) and (C), respectively, with n ≧ 100. Data were analyzed using unpaired two-tailed t -test and presented as mean ± SEM Scale bar, 10 μm. ( D ) Co-immunoprecipitation of endogenous BTG3 and XPC from HaCaT cells. ( E, F ) Retention of XPC at localized UV damage in BTG3 KO cells. Localized UVC-irradiation (100 J/m 2 ) was performed with 5 μM isopore membrane filter and XPC loading at localized UV damage sites was assessed using confocal microscopy (E). Scale bar, 10 μm. Percent cells with XPC-positive foci were counted and presented as mean ± SEM in panel (F). Data were analyzed using unpaired two-tailed t -test. n ≧ 50. ( G, H ) Mobility of XPC was reduced in BTG3 KO cells. The mobility of XPC-GFP in mock-treated or global UV-irradiated (20 J/m 2 ) parental and BTG3 KO HEK293T cells was assessed using FRAP. Fluorescence recovery was monitored over 120 s and normalized to prebleach intensity ( n = 36 from 3 independent experiments) (G). Data were analyzed using unpaired two-tailed t -tests and shown as mean ± SEM in panel (H).

    Article Snippet: After incubation with PLA blocking solution, HaCaT cells were incubated with anti-XPC (Santa Cruz, 1:200 dilution) and anti-BTG3 (Lab raised, 1:100 dilution) antibodies overnight at 4°C with gentle rocking.

    Techniques: Fluorescence, Two Tailed Test, Immunoprecipitation, Irradiation, Membrane, Confocal Microscopy