| ERCC6L facilitates the onset of mammary neoplasia and promotes the high malignance of breast cancer by accelerating the cell cycle. | ERCC6L facilitates the onset of mammary neoplasia and promotes the high malignance of breast cancer by accelerating the cell cycle.
Yang H, Zhen X, Yang Y, Zhang Y, Zhang S, Hao Y, Du G, Wang H, Zhang B, Li W, Wang J., Free PMC Article | 09/27/2023 |
| A pan-cancer analysis of the oncogenic role of ERCC6L. | A pan-cancer analysis of the oncogenic role of ERCC6L.
Lu Z, Fei L, Hou G., Free PMC Article | 12/31/2022 |
| Overexpression of ERCC6L correlates with poor prognosis and confers malignant phenotypes of lung adenocarcinoma. | Overexpression of ERCC6L correlates with poor prognosis and confers malignant phenotypes of lung adenocarcinoma.
Huang X, Jiang L, Lu S, Yuan M, Lin H, Li B, Wen Z, Zhong Y., Free PMC Article | 06/11/2022 |
| ERCC6L is a biomarker and therapeutic target for non-small cell lung adenocarcinoma. | ERCC6L is a biomarker and therapeutic target for non-small cell lung adenocarcinoma.
Hou G, Lu Z, Bi Y, Deng J, Yang X. | 03/26/2022 |
| ERCC6L promotes cell growth and metastasis in gastric cancer through activating NF-kappaB signaling. | ERCC6L promotes cell growth and metastasis in gastric cancer through activating NF-κB signaling.
Chen D, Liu Q, Cao G., Free PMC Article | 01/22/2022 |
| Development and validation of hub genes for lymph node metastasis in patients with prostate cancer. | Development and validation of hub genes for lymph node metastasis in patients with prostate cancer.
Xu N, Chen SH, Lin TT, Cai H, Ke ZB, Dong RN, Huang P, Li XD, Chen YH, Zheng QS., Free PMC Article | 05/1/2021 |
| ERCC6L promotes the progression of hepatocellular carcinoma through activating PI3K/AKT and NF-kappaB signaling pathway. | ERCC6L promotes the progression of hepatocellular carcinoma through activating PI3K/AKT and NF-κB signaling pathway.
Chen H, Wang H, Yu X, Zhou S, Zhang Y, Wang Z, Huang S, Wang Z., Free PMC Article | 04/24/2021 |
| The ZATT-TOP2A-PICH Axis Drives Extensive Replication Fork Reversal to Promote Genome Stability. | The ZATT-TOP2A-PICH Axis Drives Extensive Replication Fork Reversal to Promote Genome Stability.
Tian T, Bu M, Chen X, Ding L, Yang Y, Han J, Feng XH, Xu P, Liu T, Ying S, Lei Y, Li Q, Huang J. | 02/2/2021 |
| the present study provides preliminary evidence of the promoting effect of ERCC6L on the cell viability of RCC in vitro and in vivo. Further studies of the mechanisms underlying the regulation of ERCC6L may provide novel therapeutic targets in RCC. | ERCC6L that is up-regulated in high grade of renal cell carcinoma enhances cell viability in vitro and promotes tumor growth in vivo potentially through modulating MAPK signalling pathway.
Zhang G, Yu Z, Fu S, Lv C, Dong Q, Fu C, Kong C, Zeng Y. | 07/11/2020 |
| The study shows the dependency of triple-negative breast cancer cells on PICH for faithful chromosome segregation. | Loss of PICH promotes chromosome instability and cell death in triple-negative breast cancer.
Huang Y, Li W, Yan W, Wu J, Chen L, Yao X, Gu F, Lv L, Zhao J, Zhao M, Xia T, Han Q, Li T, Ying X, Li T, Xia Q, Li A, Zhang X, Chen Y, Zhou T., Free PMC Article | 07/11/2020 |
| These findings suggested that ERCC6L, which is highly expressed in breast cancer, acts as an oncogene, is involved in breast cancer development and may serve as a novel molecular target for the treatment of breast cancer. | shRNA knockdown of DNA helicase ERCC6L expression inhibits human breast cancer growth.
Liu J, Sun J, Zhang Q, Zeng Z. | 11/10/2018 |
| ERCC6L may stimulates cancer cell proliferation by promoting cell cycle through a way of RAB31-MAPK-CDK2, and it could be a potential biomarker for cancer prognosis and target for cancer treatment. | ERCC6L, a DNA helicase, is involved in cell proliferation and associated with survival and progress in breast and kidney cancers.
Pu SY, Yu Q, Wu H, Jiang JJ, Chen XQ, He YH, Kong QP., Free PMC Article | 04/7/2018 |
| Data indicate BEND3 as a new interaction partner for PICH in mitosis, and have defined the residues within a TPR-BEN domain interface that mediate this interaction. | A novel TPR-BEN domain interaction mediates PICH-BEND3 association.
Pitchai GP, Kaulich M, Bizard AH, Mesa P, Yao Q, Sarlos K, Streicher WW, Nigg EA, Montoya G, Hickson ID., Free PMC Article | 12/2/2017 |
| Characterization of the NTPR and BD1 interacting domains of the human PICH-BEND3 complex has been reported. | Characterization of the NTPR and BD1 interacting domains of the human PICH-BEND3 complex.
Pitchai GP, Hickson ID, Streicher W, Montoya G, Mesa P., Free PMC Article | 11/25/2017 |
| the mitotic roles of PICH and explore further the role of PICH in the timely segregation of the ribosomal DNA locus, are reported. | PICH promotes mitotic chromosome segregation: Identification of a novel role in rDNA disjunction.
Nielsen CF, Hickson ID., Free PMC Article | 06/24/2017 |
| a novel SUMO-dependent regulation of PICH's function on mitotic centromeres, is reported. | SUMO-interacting motifs (SIMs) in Polo-like kinase 1-interacting checkpoint helicase (PICH) ensure proper chromosome segregation during mitosis.
Sridharan V, Azuma Y., Free PMC Article | 06/24/2017 |
| PICH and Topo II cooperate to prevent chromosome missegregation events in mitosis. | PICH promotes sister chromatid disjunction and co-operates with topoisomerase II in mitosis.
Nielsen CF, Huttner D, Bizard AH, Hirano S, Li TN, Palmai-Pallag T, Bjerregaard VA, Liu Y, Nigg EA, Wang LH, Hickson ID., Free PMC Article | 05/14/2016 |
| PICH is a SUMO-interacting protein and a mitotic SUMO substrate. | SUMOylation regulates polo-like kinase 1-interacting checkpoint helicase (PICH) during mitosis.
Sridharan V, Park H, Ryu H, Azuma Y., Free PMC Article | 05/9/2015 |
| PICH recognizes and stabilizes DNA under tension during anaphase, thereby facilitating the resolution of entangled sister chromatids. | PICH: a DNA translocase specially adapted for processing anaphase bridge DNA.
Biebricher A, Hirano S, Enzlin JH, Wiechens N, Streicher WW, Huttner D, Wang LH, Nigg EA, Owen-Hughes T, Liu Y, Peterman E, Wuite GJL, Hickson ID., Free PMC Article | 01/11/2014 |
| PICH protein was required for the correct recruitment to the centromere of active topoisomerase IIalpha, an enzyme specialized in the catenation/decatenation process. | Bloom's syndrome and PICH helicases cooperate with topoisomerase IIα in centromere disjunction before anaphase.
Rouzeau S, Cordelières FP, Buhagiar-Labarchède G, Hurbain I, Onclercq-Delic R, Gemble S, Magnaghi-Jaulin L, Jaulin C, Amor-Guéret M., Free PMC Article | 09/22/2012 |
| PICH binds to BLM and enables BLM localization to anaphase centromeric threads. PICH and BLM unravel centromeric chromatin and keep anaphase DNA threads mostly free of nucleosomes. | PICH and BLM limit histone association with anaphase centromeric DNA threads and promote their resolution.
Ke Y, Huh JW, Warrington R, Li B, Wu N, Leng M, Zhang J, Ball HL, Li B, Yu H., Free PMC Article | 11/5/2011 |
| the PICH-Plk1 complex plays a critical role in maintaining prometaphase chromosome architecture | PICH and cotargeted Plk1 coordinately maintain prometaphase chromosome arm architecture.
Kurasawa Y, Yu-Lee LY., Free PMC Article | 08/9/2010 |
| the spindle checkpoint failure formerly attributed to the depletion of PICH most likely reflects an off-target effect that causes the lowering of Mad2 transcript and protein. | Re-examination of siRNA specificity questions role of PICH and Tao1 in the spindle checkpoint and identifies Mad2 as a sensitive target for small RNAs.
Hübner NC, Wang LH, Kaulich M, Descombes P, Poser I, Nigg EA., Free PMC Article | 06/28/2010 |
| PICH phosphorylation and its ATPase activity are required for mitotic chromosome compaction through the targeting of Plk1 to chromosome arms. | Targeting Plk1 to chromosome arms and regulating chromosome compaction by the PICH ATPase.
Leng M, Besusso D, Jung SY, Wang Y, Qin J. | 01/21/2010 |
| The sensitivity to depletion of topo IIalpha might be linked to structural alterations within the centromere domain, indicated by shortening of the distance across metaphase sister centromeres and persistence of PICH-coated connections. | Depletion of topoisomerase IIalpha leads to shortening of the metaphase interkinetochore distance and abnormal persistence of PICH-coated anaphase threads.
Spence JM, Phua HH, Mills W, Carpenter AJ, Porter AC, Farr CJ., Free PMC Article | 01/21/2010 |