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anti fancd2  (Novus Biologicals)


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    Structured Review

    Novus Biologicals anti fancd2
    Anti Fancd2, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 32 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/fancd2/FANCD2+Antibody+(FI-17)/us12558369-285-24-25
    Average 94 stars, based on 32 article reviews
    anti fancd2 - by Bioz Stars, 2026-09
    94/100 stars

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    Related Articles

    Incubation:

    Article Title: TSN Disrupts Fanconi Anemia Pathway Activation Through JAK/STAT1-Mediated Transcriptional Repression of FA Core Subunits in Bladder Cancer
    Article Snippet: Equal amounts of 40 μg protein were separated by SDS-PAGE and transferred onto PVDF membranes (P0021S-1L, Beyotime). .. Membranes were blocked with 5% non-fat milk in TBST for 1 h at room temperature and incubated overnight at 4°C with primary antibodies against FANCI (20789-1-AP, Proteintech, China, 1: 2000), FANCD2 (NB100-316, Novus Biologicals, USA, 1: 2000), β-Actin (AC026, ABclonal, China, 1: 2000), FANCL (A6812, ABclonal, 1: 2000), FANCB (A2435, ABclonal, 1: 2000), FAAP100 (A8591, ABclonal, 1: 2000), FANCA (A9529, ABclonal, 1: 2000), FANCC (A1812, ABclonal, 1: 2000), FANCF (18060-1-AP, Proteintech, 1: 2000), FANCG (A6206, ABclonal, 1: 2000), FANCM (A7602, ABclonal, 1: 2000), FAAP24 (26431-1-AP, Proteintech, 1: 2000), p-SMAD2 (80427-2-RR, Proteintech, 1: 2000), SMAD2 (67343-1-Ig, Proteintech, 1: 2000), p-STAT1 (82674-10-RR, Proteintech, 1: 2000), STAT1 (66545-1-Ig, Proteintech, 1: 2000), p-ERK1/2 (80031-1-RR, Proteintech, 1: 2000), ERK1/2 (11257-1-AP, Proteintech, 1: 2000). .. After washing, membranes were incubated with HRP-conjugated goat anti rabbit IgG (SA00001-2, Proteintech, 1: 5000) or HRP-conjugated goat anti-mouse IgG (SA00001-1, Proteintech, 1: 5000) for 1 h at room temperature.

    Proximity Ligation Assay:

    Article Title: FANCD2 restrains fork progression and prevents fragility at early origins upon re-replication
    Article Snippet: .. The PLA reaction was performed using the following reagents: PCNA (PC10, sc-56, Santa Cruz), MCM2 (D7G11, 3619, Cell Signaling), FANCD2 (NB100-182, Novus Biologicals), anti-Biotin (200-002-211, Jackson ImmunoResearch), Duolink in situ PLA probe anti-rabbit PLUS (Merck, DUO92002), Duolink in situ PLA probe anti-mouse MINUS (Merck, DUO92004) and Duolink-Detection Reagents Red (Merck). .. Finally, nuclei were stained with DAPI and mounted with MOWIOL® 4–88. (Sigma-Aldrich).

    In Situ:

    Article Title: FANCD2 restrains fork progression and prevents fragility at early origins upon re-replication
    Article Snippet: .. The PLA reaction was performed using the following reagents: PCNA (PC10, sc-56, Santa Cruz), MCM2 (D7G11, 3619, Cell Signaling), FANCD2 (NB100-182, Novus Biologicals), anti-Biotin (200-002-211, Jackson ImmunoResearch), Duolink in situ PLA probe anti-rabbit PLUS (Merck, DUO92002), Duolink in situ PLA probe anti-mouse MINUS (Merck, DUO92004) and Duolink-Detection Reagents Red (Merck). .. Finally, nuclei were stained with DAPI and mounted with MOWIOL® 4–88. (Sigma-Aldrich).

    Immunostaining:

    Article Title: The SMC5/SMC6 complex is critical for resolving R-loop-induced transcription–replication conflicts
    Article Snippet: .. Primary antibodies used for immunostaining: S9.6 antibody (ENH001, Kerafast), FANCD2 (NB100-182SS, Novus Biologicals), and γH2AX (07164, Upstate). ..



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    Replication stress and DNA damage response at CTCF/cohesin-binding sites in normal cells (A–D) ChIP-seq signal profile and heatmap of (A) MRE11, (B) STN1+HU 3h, (C) γH2AX (normalized with H2AX), and (D) RAD51 in the Mid S phase of HeLa cells plotted at CBSs shared between HeLa and normal cells (H1, IMR90, and RPE1 cells) (12,517 sites) and HeLa-specific CBSs (2,293 sites) and normal-specific sites (13,702). For the γH2AX signal ±10 kb flanks were considered, while for others the signal is plotted at ±5 kb regions. (E–H) ChIP-qPCR plots of (E) MRE11, (F) <t>FANCD2,</t> (G) γH2AX, and (H) RAD51 in Mid S synchronized hTERT RPE-1 cells at CBSs and CTCF-unbound sites. The y axis (fold enrichment over beads) indicates the % input in immunoprecipitation divided by that of beads. The bar represents the mean value from three replicates, and the error bar represents the standard error of the mean. Statistical significance was determined by using a two-sided Mann-Whitney U test.
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    Replication stress and DNA damage response at CTCF/cohesin-binding sites in normal cells (A–D) ChIP-seq signal profile and heatmap of (A) MRE11, (B) STN1+HU 3h, (C) γH2AX (normalized with H2AX), and (D) RAD51 in the Mid S phase of HeLa cells plotted at CBSs shared between HeLa and normal cells (H1, IMR90, and RPE1 cells) (12,517 sites) and HeLa-specific CBSs (2,293 sites) and normal-specific sites (13,702). For the γH2AX signal ±10 kb flanks were considered, while for others the signal is plotted at ±5 kb regions. (E–H) ChIP-qPCR plots of (E) MRE11, (F) <t>FANCD2,</t> (G) γH2AX, and (H) RAD51 in Mid S synchronized hTERT RPE-1 cells at CBSs and CTCF-unbound sites. The y axis (fold enrichment over beads) indicates the % input in immunoprecipitation divided by that of beads. The bar represents the mean value from three replicates, and the error bar represents the standard error of the mean. Statistical significance was determined by using a two-sided Mann-Whitney U test.
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    Image Search Results


    Inhibition of NAMPT function via KPT-9274 inhibits tumor growth in vivo. (A) NOG mice were injected subcutaneously with Mino cells. After detection of the tumor, the mice were randomized and treated orally with either KPT-9274 or the vehicle for 5 consecutive days per week for 3 weeks. Tumor volume was evaluated via caliper measurement. Differences between the 2 groups were evaluated using the standard t test. (B) Tumor cells collected from mice were lysed in radio-immunoprecipitation assay buffer, and the whole-cell lysate was subjected to WB analysis and probed with antibodies against Cl-PARP, FANCD2, RAD51, and γ-H2AX. GAPDH was used as the loading control. ns > .05; ∗∗ P ≤ .01; ∗∗∗ P ≤ .001; ∗∗∗∗ P ≤ .0001.

    Journal: Blood Advances

    Article Title: Inhibition of NAMPT targets DNA damage response to sensitize alkylating chemotherapy in TP53 mutant mantle cell lymphoma ∗

    doi: 10.1182/bloodadvances.2025016765

    Figure Lengend Snippet: Inhibition of NAMPT function via KPT-9274 inhibits tumor growth in vivo. (A) NOG mice were injected subcutaneously with Mino cells. After detection of the tumor, the mice were randomized and treated orally with either KPT-9274 or the vehicle for 5 consecutive days per week for 3 weeks. Tumor volume was evaluated via caliper measurement. Differences between the 2 groups were evaluated using the standard t test. (B) Tumor cells collected from mice were lysed in radio-immunoprecipitation assay buffer, and the whole-cell lysate was subjected to WB analysis and probed with antibodies against Cl-PARP, FANCD2, RAD51, and γ-H2AX. GAPDH was used as the loading control. ns > .05; ∗∗ P ≤ .01; ∗∗∗ P ≤ .001; ∗∗∗∗ P ≤ .0001.

    Article Snippet: Western blotting (WB) was performed to evaluate the expression levels of total protein and phospho-specific isoforms using the following antibodies: FANCD2 (Santa Cruz Biotechnology, sc-20022), RAD51 (Santa Cruz Biotechnology, sc-398587), PBEF (Santa Cruz Biotechnology, sc-166946), cleaved Caspase3 (Cell Signaling Technology, 9664s), PARP (Cell Signaling Technology, 9532s), cleaved PARP (Cell Signaling Technology, 5625s), γ-H2AX (Ser139; Cell Signaling Technology, 9718s), p-CHK1 (Ser345; Cell Signaling Technology, 2341s), p53 (Cell Signaling Technology, 2527s), p-ATR (Ser428; Cell Signaling Technology, 2853s), p-ATM (Ser1981; Cell Signaling Technology, 4526s), and p-CHK2 (Thr68; Cell Signaling Technology, 2197s).

    Techniques: Inhibition, In Vivo, Injection, Radio Immunoprecipitation, Control

    Inhibition of NAMPT function via KPT-9274 inhibits tumor growth in vivo. (A) NOG mice were injected subcutaneously with Mino cells. After detection of the tumor, the mice were randomized and treated orally with either KPT-9274 or the vehicle for 5 consecutive days per week for 3 weeks. Tumor volume was evaluated via caliper measurement. Differences between the 2 groups were evaluated using the standard t test. (B) Tumor cells collected from mice were lysed in radio-immunoprecipitation assay buffer, and the whole-cell lysate was subjected to WB analysis and probed with antibodies against Cl-PARP, FANCD2, RAD51, and γ-H2AX. GAPDH was used as the loading control. ns > .05; ∗∗ P ≤ .01; ∗∗∗ P ≤ .001; ∗∗∗∗ P ≤ .0001.

    Journal: Blood Advances

    Article Title: Inhibition of NAMPT targets DNA damage response to sensitize alkylating chemotherapy in TP53 mutant mantle cell lymphoma ∗

    doi: 10.1182/bloodadvances.2025016765

    Figure Lengend Snippet: Inhibition of NAMPT function via KPT-9274 inhibits tumor growth in vivo. (A) NOG mice were injected subcutaneously with Mino cells. After detection of the tumor, the mice were randomized and treated orally with either KPT-9274 or the vehicle for 5 consecutive days per week for 3 weeks. Tumor volume was evaluated via caliper measurement. Differences between the 2 groups were evaluated using the standard t test. (B) Tumor cells collected from mice were lysed in radio-immunoprecipitation assay buffer, and the whole-cell lysate was subjected to WB analysis and probed with antibodies against Cl-PARP, FANCD2, RAD51, and γ-H2AX. GAPDH was used as the loading control. ns > .05; ∗∗ P ≤ .01; ∗∗∗ P ≤ .001; ∗∗∗∗ P ≤ .0001.

    Article Snippet: Western blotting (WB) was performed to evaluate the expression levels of total protein and phospho-specific isoforms using the following antibodies: FANCD2 (Santa Cruz Biotechnology, sc-20022), RAD51 (Santa Cruz Biotechnology, sc-398587), PBEF (Santa Cruz Biotechnology, sc-166946), cleaved Caspase3 (Cell Signaling Technology, 9664s), PARP (Cell Signaling Technology, 9532s), cleaved PARP (Cell Signaling Technology, 5625s), γ-H2AX (Ser139; Cell Signaling Technology, 9718s), p-CHK1 (Ser345; Cell Signaling Technology, 2341s), p53 (Cell Signaling Technology, 2527s), p-ATR (Ser428; Cell Signaling Technology, 2853s), p-ATM (Ser1981; Cell Signaling Technology, 4526s), and p-CHK2 (Thr68; Cell Signaling Technology, 2197s).

    Techniques: Inhibition, In Vivo, Injection, Radio Immunoprecipitation, Control

    Replication stress and DNA damage response at CTCF/cohesin-binding sites in normal cells (A–D) ChIP-seq signal profile and heatmap of (A) MRE11, (B) STN1+HU 3h, (C) γH2AX (normalized with H2AX), and (D) RAD51 in the Mid S phase of HeLa cells plotted at CBSs shared between HeLa and normal cells (H1, IMR90, and RPE1 cells) (12,517 sites) and HeLa-specific CBSs (2,293 sites) and normal-specific sites (13,702). For the γH2AX signal ±10 kb flanks were considered, while for others the signal is plotted at ±5 kb regions. (E–H) ChIP-qPCR plots of (E) MRE11, (F) FANCD2, (G) γH2AX, and (H) RAD51 in Mid S synchronized hTERT RPE-1 cells at CBSs and CTCF-unbound sites. The y axis (fold enrichment over beads) indicates the % input in immunoprecipitation divided by that of beads. The bar represents the mean value from three replicates, and the error bar represents the standard error of the mean. Statistical significance was determined by using a two-sided Mann-Whitney U test.

    Journal: iScience

    Article Title: CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cells

    doi: 10.1016/j.isci.2026.114646

    Figure Lengend Snippet: Replication stress and DNA damage response at CTCF/cohesin-binding sites in normal cells (A–D) ChIP-seq signal profile and heatmap of (A) MRE11, (B) STN1+HU 3h, (C) γH2AX (normalized with H2AX), and (D) RAD51 in the Mid S phase of HeLa cells plotted at CBSs shared between HeLa and normal cells (H1, IMR90, and RPE1 cells) (12,517 sites) and HeLa-specific CBSs (2,293 sites) and normal-specific sites (13,702). For the γH2AX signal ±10 kb flanks were considered, while for others the signal is plotted at ±5 kb regions. (E–H) ChIP-qPCR plots of (E) MRE11, (F) FANCD2, (G) γH2AX, and (H) RAD51 in Mid S synchronized hTERT RPE-1 cells at CBSs and CTCF-unbound sites. The y axis (fold enrichment over beads) indicates the % input in immunoprecipitation divided by that of beads. The bar represents the mean value from three replicates, and the error bar represents the standard error of the mean. Statistical significance was determined by using a two-sided Mann-Whitney U test.

    Article Snippet: Antibodies used are: CTCF (3418: Cell Signaling Technology, 1 μg), RAD21 (ab992: Abcam, 1 μg), MRE11 (ab208020: Abcam, 2 μg), γH2AX (ab81299: Abcam, 2 μg), H2AX (ab11175: Abcam, 2 μg), RAD51 (ab176458: Abcam, 2 μg), ATM (ab201022: Abcam, 2 μg) and FANCD2 (NB100-182: Novus Biologicals, 2 μg).

    Techniques: Binding Assay, ChIP-sequencing, ChIP-qPCR, Immunoprecipitation, MANN-WHITNEY