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Fig. <t>6</t> <t>AMBRA1</t> tumor suppressor activity is associated with regulation of G2/M phase mediators. A Volcano plots showing changes in protein levels for 39 cell cycle-associated regulators in ATRT cells upon loss of AMBRA1 as assessed by DigiWest. Left, common changes in protein levels across four ATRT cell lines upon AMBRA1 knockout. Right, context-specific changes in protein levels in AMBRA1 responder (CHLA06 and CHLA266) as compared to AMBRA1 non-responder ATRT cell lines (BT12 and BT16) upon loss of AMBRA1. B Western blot analyses for control and sgAMBRA1 CHLA06 cells with or without overexpression of <t>AURKA</t> (AURKA OE). Note AURKA and CDK1 overexpression driven by loss of AMBRA1 alone. C Effect of gain of AURKA on the proliferation of ATRT cells on control and sgAMBRA1 background. D Effect of gain of AURKA on cell cycle phase distributions of control and sgAMBRA1 ATRT cells. Data are shown as mean ± SD (B). Statistics are derived from and Welch’s t tests (A), and from paired t tests (C)
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Fig. 6 AMBRA1 tumor suppressor activity is associated with regulation of G2/M phase mediators. A Volcano plots showing changes in protein levels for 39 cell cycle-associated regulators in ATRT cells upon loss of AMBRA1 as assessed by DigiWest. Left, common changes in protein levels across four ATRT cell lines upon AMBRA1 knockout. Right, context-specific changes in protein levels in AMBRA1 responder (CHLA06 and CHLA266) as compared to AMBRA1 non-responder ATRT cell lines (BT12 and BT16) upon loss of AMBRA1. B Western blot analyses for control and sgAMBRA1 CHLA06 cells with or without overexpression of AURKA (AURKA OE). Note AURKA and CDK1 overexpression driven by loss of AMBRA1 alone. C Effect of gain of AURKA on the proliferation of ATRT cells on control and sgAMBRA1 background. D Effect of gain of AURKA on cell cycle phase distributions of control and sgAMBRA1 ATRT cells. Data are shown as mean ± SD (B). Statistics are derived from and Welch’s t tests (A), and from paired t tests (C)

Journal: Genome biology

Article Title: Functional screening reveals genetic dependencies and diverging cell cycle control in atypical teratoid rhabdoid tumors.

doi: 10.1186/s13059-024-03438-w

Figure Lengend Snippet: Fig. 6 AMBRA1 tumor suppressor activity is associated with regulation of G2/M phase mediators. A Volcano plots showing changes in protein levels for 39 cell cycle-associated regulators in ATRT cells upon loss of AMBRA1 as assessed by DigiWest. Left, common changes in protein levels across four ATRT cell lines upon AMBRA1 knockout. Right, context-specific changes in protein levels in AMBRA1 responder (CHLA06 and CHLA266) as compared to AMBRA1 non-responder ATRT cell lines (BT12 and BT16) upon loss of AMBRA1. B Western blot analyses for control and sgAMBRA1 CHLA06 cells with or without overexpression of AURKA (AURKA OE). Note AURKA and CDK1 overexpression driven by loss of AMBRA1 alone. C Effect of gain of AURKA on the proliferation of ATRT cells on control and sgAMBRA1 background. D Effect of gain of AURKA on cell cycle phase distributions of control and sgAMBRA1 ATRT cells. Data are shown as mean ± SD (B). Statistics are derived from and Welch’s t tests (A), and from paired t tests (C)

Article Snippet: Primary antibodies used in this study for DigiWest were the following: β-actin (Sigma, A1978, AMBRA1 (Cell Signaling, 24907), ATM (Cell Signaling, 2873), ATR (Cell Signaling, 2790), AURKA (Cell Signaling, 4718), AURKB (Cell Signaling, 3094), BUB1B (Cell Signaling, 5421), Caspase3 (Cell Signaling, 9662), CDK1 (Cell Signaling, 9112), CDK1-pTyr15 (Cell Signaling, 4539), CDC25A (abm, Y021163), CDC25A-pSer75 (abm, Y011138), CDC25B (R&D, AF1649), CDC27 (Transduction Laboratories, C40920), CDK2 (Cell Signaling, 2546), CDK2-pThr160 (Cell Signaling, 2561), CDK3 (abcam, ab135805), CDK4 (Cell Signaling, 2906), CDK4-pThr172 (Invitrogen, PA-64482), CDK5 (Cell Signaling, 2506), CDK6 (Cell Signaling, 13331), CDK6-pTyr13 (biorbyt, orb15013), CDK6-pTyr24 (biorbyt, orb15014), CHK2 (Cell Signaling, 3440), CHK2-pThr68 (Cell Signaling, 2661), c-MYC (Cell Signaling, 9402), c-MYC-pThr58 (ThermoFisher, PA5-37654), c-MYC-pThr62/Ser62 (abcam, ab32029), cyclin A (abcam, ab53054), cyclin B1 (abcam, ab32053), cyclin D1 (Cell Signaling, 2926), cyclin D1-pThr286 (ThermoFisher, PA5-37487), cyclin D2 (Cell Signaling, 3741), cyclin D3 (Cell Signaling, 2936), cyclin E1 (Cell Signaling, 4129), cyclin E2 (Cell Signaling, 4132), E2F-2 (Millipore, DR1095), E2F-4 (biorbyt, orb10571), histone H3-pSer28 (Millipore, 07–145), hisotne H3-pSer10 (Cell Signaling, 9701), MCM2 (Cell Signaling, 3619), MCM2-pSer139 (Cell Signaling, 8861), MDM2 (Santa Cruz, sc-965), MDM2-pSer166 (Cell Signaling, 3521), p16 (ProteinTech Group, 10883-1-AP), p21 (Cell Signaling, 2947), p27 (Cell Signaling, 3698), p53 (Santa Cruz, sc-126), p53-pSer37 (Cell Signaling, 9289), p53-pSer15 (Cell Signaling, 9284), RB (Cell Signaling, 9313), RB-pSer807/Ser811 (Cell Signaling, 8516), RB-pSer780 (Cell Signaling, 3590), RB-pSer608 (Cell Signaling, 8147), RB-pSer795 (Cell Signaling, 9301), RBPSUH (Cell Signaling, 5313), RPA2 p34 (Millipore, 04–1481), Survivin (Cell Signaling, 2802), TOPK (Cell Signaling, 4942), and TOPO 2 alpha (Santa Cruz, sc-13058).

Techniques: Activity Assay, Knock-Out, Western Blot, Control, Over Expression, Derivative Assay

Fig. 7 AMBRA1 regulates ubiquitin-dependent degradation of aurora kinases in a context-dependent manner. A Complex structure prediction using AlphaFold2_mmseqs2 for AMBRA1WD40 with DDB1, cyclin D1, AURKA or AURKB. Top, cartoon illustration of predicted heteromeric protein complexes. Interchain AlphaFold2 contacts (< 8 Å) are shown as straight lines colored by predicted alignment error (PAE). AMBRA1 residues implicated in DDB1 binding are highlighted in green. Predicted template modeling scores (pTM) are indicated. Bottom, pairwise PAE scores for all protein complexes. B Heat map showing log2 fold changes of label-free quantification values from FLAG affinity purification and mass spectrometry detection in AMBRA-FLAG versus FLAG expressing ATRT cells. Cells were investigated with and without treatment of the CRL inhibitor MLN4924. C Co-immunoprecipitation analyses followed by western blot for selected potential AMBRA1 interactors and substrates. Previously identified interactors and substrates of AMBRA1 (CUL4A, DDB1, and cyclin D1) were included as controls. D Top: Immunoassays of cyclin D1, cyclin D3, AURKA, and AURKB for BT12 and CHLA06 cells, both in wildtype and AMBRA1-knockout conditions. Cells were treated with DMSO, 0.4 μM Baf-A1, or 1 μM MLN4924 for 4 h (cyclin D) or 12 h (aurora kinases). Increase in LC3B-II levels was used as a validation of autophagy inhibition. Bottom: Quantification of protein expression levels relative the corresponding DMSO control conditions. E Left: Immunoassays from His pull-down experiments for BT12 and CHLA266 cells, both in wildtype and AMBRA1-knockout conditions, transfected either with 6xHis-empty or 6xHis-tagged ubiquitin 48 h prior to pull-down. Right: Quantification of AURKA and AURKB ubiquitylation relative to total protein levels. F Model of context-dependent, CRL4AMBRA1-associated blockade of cell cycle regulators via degradation by the ubiquitin-proteasome system. Data are shown as mean ± SD (D, E). Statistics are derived from two-way ANOVA tests with Dunnett’s (D) or Sidak’s correction (E). *P < 0.05, **P < 0.01,***P < 0.001, ****P < 0.0001

Journal: Genome biology

Article Title: Functional screening reveals genetic dependencies and diverging cell cycle control in atypical teratoid rhabdoid tumors.

doi: 10.1186/s13059-024-03438-w

Figure Lengend Snippet: Fig. 7 AMBRA1 regulates ubiquitin-dependent degradation of aurora kinases in a context-dependent manner. A Complex structure prediction using AlphaFold2_mmseqs2 for AMBRA1WD40 with DDB1, cyclin D1, AURKA or AURKB. Top, cartoon illustration of predicted heteromeric protein complexes. Interchain AlphaFold2 contacts (< 8 Å) are shown as straight lines colored by predicted alignment error (PAE). AMBRA1 residues implicated in DDB1 binding are highlighted in green. Predicted template modeling scores (pTM) are indicated. Bottom, pairwise PAE scores for all protein complexes. B Heat map showing log2 fold changes of label-free quantification values from FLAG affinity purification and mass spectrometry detection in AMBRA-FLAG versus FLAG expressing ATRT cells. Cells were investigated with and without treatment of the CRL inhibitor MLN4924. C Co-immunoprecipitation analyses followed by western blot for selected potential AMBRA1 interactors and substrates. Previously identified interactors and substrates of AMBRA1 (CUL4A, DDB1, and cyclin D1) were included as controls. D Top: Immunoassays of cyclin D1, cyclin D3, AURKA, and AURKB for BT12 and CHLA06 cells, both in wildtype and AMBRA1-knockout conditions. Cells were treated with DMSO, 0.4 μM Baf-A1, or 1 μM MLN4924 for 4 h (cyclin D) or 12 h (aurora kinases). Increase in LC3B-II levels was used as a validation of autophagy inhibition. Bottom: Quantification of protein expression levels relative the corresponding DMSO control conditions. E Left: Immunoassays from His pull-down experiments for BT12 and CHLA266 cells, both in wildtype and AMBRA1-knockout conditions, transfected either with 6xHis-empty or 6xHis-tagged ubiquitin 48 h prior to pull-down. Right: Quantification of AURKA and AURKB ubiquitylation relative to total protein levels. F Model of context-dependent, CRL4AMBRA1-associated blockade of cell cycle regulators via degradation by the ubiquitin-proteasome system. Data are shown as mean ± SD (D, E). Statistics are derived from two-way ANOVA tests with Dunnett’s (D) or Sidak’s correction (E). *P < 0.05, **P < 0.01,***P < 0.001, ****P < 0.0001

Article Snippet: Primary antibodies used in this study for DigiWest were the following: β-actin (Sigma, A1978, AMBRA1 (Cell Signaling, 24907), ATM (Cell Signaling, 2873), ATR (Cell Signaling, 2790), AURKA (Cell Signaling, 4718), AURKB (Cell Signaling, 3094), BUB1B (Cell Signaling, 5421), Caspase3 (Cell Signaling, 9662), CDK1 (Cell Signaling, 9112), CDK1-pTyr15 (Cell Signaling, 4539), CDC25A (abm, Y021163), CDC25A-pSer75 (abm, Y011138), CDC25B (R&D, AF1649), CDC27 (Transduction Laboratories, C40920), CDK2 (Cell Signaling, 2546), CDK2-pThr160 (Cell Signaling, 2561), CDK3 (abcam, ab135805), CDK4 (Cell Signaling, 2906), CDK4-pThr172 (Invitrogen, PA-64482), CDK5 (Cell Signaling, 2506), CDK6 (Cell Signaling, 13331), CDK6-pTyr13 (biorbyt, orb15013), CDK6-pTyr24 (biorbyt, orb15014), CHK2 (Cell Signaling, 3440), CHK2-pThr68 (Cell Signaling, 2661), c-MYC (Cell Signaling, 9402), c-MYC-pThr58 (ThermoFisher, PA5-37654), c-MYC-pThr62/Ser62 (abcam, ab32029), cyclin A (abcam, ab53054), cyclin B1 (abcam, ab32053), cyclin D1 (Cell Signaling, 2926), cyclin D1-pThr286 (ThermoFisher, PA5-37487), cyclin D2 (Cell Signaling, 3741), cyclin D3 (Cell Signaling, 2936), cyclin E1 (Cell Signaling, 4129), cyclin E2 (Cell Signaling, 4132), E2F-2 (Millipore, DR1095), E2F-4 (biorbyt, orb10571), histone H3-pSer28 (Millipore, 07–145), hisotne H3-pSer10 (Cell Signaling, 9701), MCM2 (Cell Signaling, 3619), MCM2-pSer139 (Cell Signaling, 8861), MDM2 (Santa Cruz, sc-965), MDM2-pSer166 (Cell Signaling, 3521), p16 (ProteinTech Group, 10883-1-AP), p21 (Cell Signaling, 2947), p27 (Cell Signaling, 3698), p53 (Santa Cruz, sc-126), p53-pSer37 (Cell Signaling, 9289), p53-pSer15 (Cell Signaling, 9284), RB (Cell Signaling, 9313), RB-pSer807/Ser811 (Cell Signaling, 8516), RB-pSer780 (Cell Signaling, 3590), RB-pSer608 (Cell Signaling, 8147), RB-pSer795 (Cell Signaling, 9301), RBPSUH (Cell Signaling, 5313), RPA2 p34 (Millipore, 04–1481), Survivin (Cell Signaling, 2802), TOPK (Cell Signaling, 4942), and TOPO 2 alpha (Santa Cruz, sc-13058).

Techniques: Ubiquitin Proteomics, Binding Assay, Quantitative Proteomics, Affinity Purification, Mass Spectrometry, Expressing, Immunoprecipitation, Western Blot, Knock-Out, Biomarker Discovery, Inhibition, Control, Transfection, Derivative Assay

Fig. 8 Inhibition of AURKA is synthetic lethal upon oncogenic loss of AMBRA1. A Dose response analyses for the AURKA inhibitor LY3295668 in AMBRA1 proficient and knockout ATRT cells. B Duration of mitosis in BT12 and CHLA06 cells, both AMBRA1 proficient and knockout cells, treated with 200 nM LY3295668. C Drug synergies as determined by the Bliss model for the combination of the CDK4/6 inhibitor abemaciclib and the AURKA inhibitor LY3295668 in AMBRA1 proficient and knockout ATRT cells. Data are shown as mean ± SD (B, D). Statistics are derived from paired t test (B), and two-way ANOVA test for interaction (E)

Journal: Genome biology

Article Title: Functional screening reveals genetic dependencies and diverging cell cycle control in atypical teratoid rhabdoid tumors.

doi: 10.1186/s13059-024-03438-w

Figure Lengend Snippet: Fig. 8 Inhibition of AURKA is synthetic lethal upon oncogenic loss of AMBRA1. A Dose response analyses for the AURKA inhibitor LY3295668 in AMBRA1 proficient and knockout ATRT cells. B Duration of mitosis in BT12 and CHLA06 cells, both AMBRA1 proficient and knockout cells, treated with 200 nM LY3295668. C Drug synergies as determined by the Bliss model for the combination of the CDK4/6 inhibitor abemaciclib and the AURKA inhibitor LY3295668 in AMBRA1 proficient and knockout ATRT cells. Data are shown as mean ± SD (B, D). Statistics are derived from paired t test (B), and two-way ANOVA test for interaction (E)

Article Snippet: Primary antibodies used in this study for DigiWest were the following: β-actin (Sigma, A1978, AMBRA1 (Cell Signaling, 24907), ATM (Cell Signaling, 2873), ATR (Cell Signaling, 2790), AURKA (Cell Signaling, 4718), AURKB (Cell Signaling, 3094), BUB1B (Cell Signaling, 5421), Caspase3 (Cell Signaling, 9662), CDK1 (Cell Signaling, 9112), CDK1-pTyr15 (Cell Signaling, 4539), CDC25A (abm, Y021163), CDC25A-pSer75 (abm, Y011138), CDC25B (R&D, AF1649), CDC27 (Transduction Laboratories, C40920), CDK2 (Cell Signaling, 2546), CDK2-pThr160 (Cell Signaling, 2561), CDK3 (abcam, ab135805), CDK4 (Cell Signaling, 2906), CDK4-pThr172 (Invitrogen, PA-64482), CDK5 (Cell Signaling, 2506), CDK6 (Cell Signaling, 13331), CDK6-pTyr13 (biorbyt, orb15013), CDK6-pTyr24 (biorbyt, orb15014), CHK2 (Cell Signaling, 3440), CHK2-pThr68 (Cell Signaling, 2661), c-MYC (Cell Signaling, 9402), c-MYC-pThr58 (ThermoFisher, PA5-37654), c-MYC-pThr62/Ser62 (abcam, ab32029), cyclin A (abcam, ab53054), cyclin B1 (abcam, ab32053), cyclin D1 (Cell Signaling, 2926), cyclin D1-pThr286 (ThermoFisher, PA5-37487), cyclin D2 (Cell Signaling, 3741), cyclin D3 (Cell Signaling, 2936), cyclin E1 (Cell Signaling, 4129), cyclin E2 (Cell Signaling, 4132), E2F-2 (Millipore, DR1095), E2F-4 (biorbyt, orb10571), histone H3-pSer28 (Millipore, 07–145), hisotne H3-pSer10 (Cell Signaling, 9701), MCM2 (Cell Signaling, 3619), MCM2-pSer139 (Cell Signaling, 8861), MDM2 (Santa Cruz, sc-965), MDM2-pSer166 (Cell Signaling, 3521), p16 (ProteinTech Group, 10883-1-AP), p21 (Cell Signaling, 2947), p27 (Cell Signaling, 3698), p53 (Santa Cruz, sc-126), p53-pSer37 (Cell Signaling, 9289), p53-pSer15 (Cell Signaling, 9284), RB (Cell Signaling, 9313), RB-pSer807/Ser811 (Cell Signaling, 8516), RB-pSer780 (Cell Signaling, 3590), RB-pSer608 (Cell Signaling, 8147), RB-pSer795 (Cell Signaling, 9301), RBPSUH (Cell Signaling, 5313), RPA2 p34 (Millipore, 04–1481), Survivin (Cell Signaling, 2802), TOPK (Cell Signaling, 4942), and TOPO 2 alpha (Santa Cruz, sc-13058).

Techniques: Inhibition, Knock-Out, Derivative Assay