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6-4pp mouse antibody  (Cosmo Bio USA)

 
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    Cosmo Bio USA 6-4pp mouse antibody
    6 4pp Mouse Antibody, supplied by Cosmo Bio USA, 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/product/6-4pp+mouse+antibody/pmc09376112__41467_2022_31820_MOESM1_ESM-58-4-8?v=Cosmo+Bio+USA
    Average 90 stars, based on 1 article reviews
    6-4pp mouse antibody - by Bioz Stars, 2026-08
    90/100 stars

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    Impairment of DNA repair synthesis and ligation inhibits repair independently of ATR. (A) Removal of 6-4PP in time was measured in the presence (■) and absence (▲) of inhibitors after global UV irradiation (30 J/m 2 ) in NHF (blue lines) and ATR-deficient cells (orange lines); NHF cells were treated with L67 for 4 h before irradiation (•). Cells were stained with a 6-4PP–specific antibody and lesion removal was measured by immunofluorescent staining and quantification of at least three independent experiments with over 40 cells per point. (B) Seckle syndrome cells (ATR) show impaired γ-H2AX staining at sites of UV damage compared with NHF. Cells were irradiated with 30 J/m 2 1 h before fixation and were processed for immunofluorescent staining with antibodies against XPB and γ-H2AX. (C) NHFs, treated and nontreated with L67 for 4 h before local UV irradiation (30 J/m 2 ), were stained for XPB and PCNA localization.

    Journal: The Journal of Cell Biology

    Article Title: Replication protein A safeguards genome integrity by controlling NER incision events

    doi: 10.1083/jcb.201006011

    Figure Lengend Snippet: Impairment of DNA repair synthesis and ligation inhibits repair independently of ATR. (A) Removal of 6-4PP in time was measured in the presence (■) and absence (▲) of inhibitors after global UV irradiation (30 J/m 2 ) in NHF (blue lines) and ATR-deficient cells (orange lines); NHF cells were treated with L67 for 4 h before irradiation (•). Cells were stained with a 6-4PP–specific antibody and lesion removal was measured by immunofluorescent staining and quantification of at least three independent experiments with over 40 cells per point. (B) Seckle syndrome cells (ATR) show impaired γ-H2AX staining at sites of UV damage compared with NHF. Cells were irradiated with 30 J/m 2 1 h before fixation and were processed for immunofluorescent staining with antibodies against XPB and γ-H2AX. (C) NHFs, treated and nontreated with L67 for 4 h before local UV irradiation (30 J/m 2 ), were stained for XPB and PCNA localization.

    Article Snippet: The following primary antibodies were used in this study: rabbit polyclonal α-XPA, α-p89 (XPB), α-ERCC1 and mouse monoclonal α-DNA Polδ (Santa Cruz Biotechnology, Inc.); mouse monoclonal α-PCNA (PC10), α-XRCC1, and α-XPA (Abcam); mouse monoclonal α-DNA ligase 3α (Genetex); mouse monoclonal α-XPG (8H7, Invitrogen); mouse monoclonal α-RPAp70 (Ab-1, Oncogene); and mouse monoclonal α-6-4PP (Cosmo Bio).

    Techniques: Ligation, Irradiation, Staining

    Prolonged accumulation of pre- and post-incision factors at NER sites in the presence of replication inhibitors. (A) Fluorescent immunostaining of XPB, RPA, Polδ, and PCNA localization at damage sites in confluent NHF after local UV irradiation (30 J/m 2 ) at time points as indicated. “Merge” refers to the combined image of DAPI and PCNA staining. (B) Immunolocalization of XPB, RPA, Polδ, and PCNA in NHF in the presence of HU and AraC at different repair times after 30 J/m 2 local UV irradiation. (C) Immunolocalization of XPB in confluent XP-A cells at different repair times after 30 J/m 2 local UV irradiation. (D) XPC and 6-4PP were visualized by immunostaining after local UV irradiation; cells were irradiated with 30 J/m 2 UV and incubated for either 30 min or 20 h.

    Journal: The Journal of Cell Biology

    Article Title: Replication protein A safeguards genome integrity by controlling NER incision events

    doi: 10.1083/jcb.201006011

    Figure Lengend Snippet: Prolonged accumulation of pre- and post-incision factors at NER sites in the presence of replication inhibitors. (A) Fluorescent immunostaining of XPB, RPA, Polδ, and PCNA localization at damage sites in confluent NHF after local UV irradiation (30 J/m 2 ) at time points as indicated. “Merge” refers to the combined image of DAPI and PCNA staining. (B) Immunolocalization of XPB, RPA, Polδ, and PCNA in NHF in the presence of HU and AraC at different repair times after 30 J/m 2 local UV irradiation. (C) Immunolocalization of XPB in confluent XP-A cells at different repair times after 30 J/m 2 local UV irradiation. (D) XPC and 6-4PP were visualized by immunostaining after local UV irradiation; cells were irradiated with 30 J/m 2 UV and incubated for either 30 min or 20 h.

    Article Snippet: The following primary antibodies were used in this study: rabbit polyclonal α-XPA, α-p89 (XPB), α-ERCC1 and mouse monoclonal α-DNA Polδ (Santa Cruz Biotechnology, Inc.); mouse monoclonal α-PCNA (PC10), α-XRCC1, and α-XPA (Abcam); mouse monoclonal α-DNA ligase 3α (Genetex); mouse monoclonal α-XPG (8H7, Invitrogen); mouse monoclonal α-RPAp70 (Ab-1, Oncogene); and mouse monoclonal α-6-4PP (Cosmo Bio).

    Techniques: Immunostaining, Irradiation, Staining, Incubation