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1

Liao, Chengcheng, Srikanth Talluri, Subodh Kumar, et al. "Base Excision Repair and Homologous Recombination Pathway Intermediates Drive Genomic Instability and Evolution in Myeloma." Blood 136, Supplement 1 (2020): 27–28. http://dx.doi.org/10.1182/blood-2020-141042.

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Multiple myeloma (MM) cells demonstrate significant genomic instability with acquisition of new genomic events over time. In an effort to decipher the pathways utilized by MM cells to genomically evolve and to acquire proliferative advantage as well as develop drug resistance, we have investigated role of various pathway intermediates. Based on our prior results showing elevated homologous recombination (HR) contributing to genomic instability and development of drug resistance, we have further studied RAD51, the key HR gene. Also based on the dysfunctional base excision repair (BER) that can
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2

Shammas, Masood, Jagannath Pal, Ankit V. Vahia, et al. "Elevated APEX1 Endonuclease Is Associated with Increased DNA Breaks and Instability in Myeloma." Blood 118, no. 21 (2011): 1805. http://dx.doi.org/10.1182/blood.v118.21.1805.1805.

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Abstract Abstract 1805 Exposure to DNA-damaging agents of both endogenous and exogenous origin, including ultraviolet (UV) radiation, give rise to apurinic/apyrimidinic (AP) or abasic sites in genome, probably the most common mutagenic DNA lesions. APEX1, the key protein involved in the repair of AP sites through base excision repair, plays an important role in the maintenance of genomic integrity. We have observed that APEX1 is overexpressed in multiple myeloma (MM) cell lines and primary cells. To evaluate its functional role MM cells were transduced with control (CS) or APEX1-specific lenti
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3

Tummanatsakun, Doungdean, Tanakorn Proungvitaya, Sittiruk Roytrakul, and Siriporn Proungvitaya. "Bioinformatic Prediction of Signaling Pathways for Apurinic/Apyrimidinic Endodeoxyribonuclease 1 (APEX1) and Its Role in Cholangiocarcinoma Cells." Molecules 26, no. 9 (2021): 2587. http://dx.doi.org/10.3390/molecules26092587.

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Apurinic/apyrimidinic endodeoxyribonuclease 1 (APEX1) is involved in the DNA damage repair pathways and associates with the metastasis of several human cancers. However, the signaling pathway of APEX1 in cholangiocarcinoma (CCA) has never been reported. In this study, to predict the signaling pathways of APEX1 and related proteins and their functions, the effects of APEX1 gene silencing on APEX1 and related protein expression in CCA cell lines were investigated using mass spectrometry and bioinformatics tools. Bioinformatic analyses predicted that APEX1 might interact with cell division cycle
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Kim, Yeo, Lim, Song, Chun, and Kim. "APEX1 Expression as a Potential Diagnostic Biomarker of Clear Cell Renal Cell Carcinoma and Hepatobiliary Carcinomas." Journal of Clinical Medicine 8, no. 8 (2019): 1151. http://dx.doi.org/10.3390/jcm8081151.

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Apurinic/apyrimidinic endonuclease 1/redox effector factor 1 (APEX1) has been known to play key roles in DNA repair, the regulation of diverse transcriptional activity, and cellular responses to redox activity. This study aimed to examine serum APEX1 (s-APEX1) expression as a possible screening biomarker for clear cell renal cell carcinoma (ccRCC), hepatocellular carcinoma (HCC), and proximal and distal cholangiocarcinoma (CC). A total of 216 frozen serum samples were collected from 39 healthy control cases, 32 patients with ≥58 copies/mL of hepatitis B viral DNA (HBV DNA (+)), 40 ccRCC cases,
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Li, Yuan, Zili Xu, Xiangyang Liu, Xiandong Peng, Shu Cao, and Zhulin Yang. "Analysis of Variance Based Significance Analysis of Cartilage Tumor." Journal of Medical Imaging and Health Informatics 10, no. 9 (2020): 1985–91. http://dx.doi.org/10.1166/jmihi.2020.3121.

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Chondrosarcoma is a malignant bone tumor with poor prognosis. Surgical treatment is the first choice for chondrosarcomas. Chondrosarcoma is not sensitive to chemotherapy and radiotherapy. Identification of biological markers is important for the early diagnosis and targeted treatment of chondrosarcoma. This study aimed to investigate the protein expression and clinicopathological significance of APEX1 and Haptoglobin in 85 chondrosarcomas and 38 osteochondromas based on deep learning. The APEX1 and Haptoglobin protein expression in tissues was measured by immunohistochemistry. The percentage o
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Kumar, Subodh, Srikanth Talluri, Mariateresa Fulciniti, Masood A. Shammas, and Nikhil C. Munshi. "Elevated APEX1 Disrupts G2/M Checkpoint, Contributing to Evolution and Survival of Myeloma Cells." Blood 126, no. 23 (2015): 2997. http://dx.doi.org/10.1182/blood.v126.23.2997.2997.

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Abstract Cell cycle checkpoints provide the cell with time to repair chromosomal DNA damage before its replication (G1) and also prior to its segregation (G2), thus ensuring integrity, maintenance and protection of genome. Although proper functioning of both checkpoints is essential, G2/M has a special significance as a potentially lethal double-strand break in DNA escape repair and persist from G2 into mitosis, it may recombine in G1 to produce gene rearrangements. Moreover, G2 is the phase where homologous recombination (HR) can utilize a sister chromatid as a template to provide error-free
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7

Tummanatsakun, Doungdean, Tanakorn Proungvitaya, Sittiruk Roytrakul, et al. "Serum Apurinic/Apyrimidinic Endodeoxyribonuclease 1 (APEX1) Level as a Potential Biomarker of Cholangiocarcinoma." Biomolecules 9, no. 9 (2019): 413. http://dx.doi.org/10.3390/biom9090413.

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Diagnostic and/or prognostic biomarkers for cholangiocarcinoma (CCA) are still insufficient with poor prognosis of patients. To discover a new CCA biomarker, we constructed our secretome database of three CCA cell lines and one control cholangiocyte cell line using GeLC-MS/MS. We selected candidate proteins by five bioinformatics tools for secretome analysis. The inclusion criteria were as follows: having predicted signal peptide or being predicted as non-classically secreted protein; together with having no transmembrane helix and being previously detected in plasma and having the highest num
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8

Kim, Daria V., Liliya M. Kulishova, Natalia A. Torgasheva, et al. "Mild phenotype of knockouts of the major apurinic/apyrimidinic endonuclease APEX1 in a non-cancer human cell line." PLOS ONE 16, no. 9 (2021): e0257473. http://dx.doi.org/10.1371/journal.pone.0257473.

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The major human apurinic/apyrimidinic (AP) site endonuclease, APEX1, is a central player in the base excision DNA repair (BER) pathway and has a role in the regulation of DNA binding by transcription factors. In vertebrates, APEX1 knockouts are embryonic lethal, and only a handful of knockout cell lines are known. To facilitate studies of multiple functions of this protein in human cells, we have used the CRISPR/Cas9 system to knock out the APEX1 gene in a widely used non-cancer hypotriploid HEK 293FT cell line. Two stable knockout lines were obtained, one carrying two single-base deletion all
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Lin, Jianhong, Chun Yang, Ariel Kwart, et al. "Apurinic/Apyrimidinic Endonuclease 1 Induced Genomic Instability Causes T-Cell Acute Lymphoblastic Leukemia in Zebrafish." Blood 126, no. 23 (2015): 1431. http://dx.doi.org/10.1182/blood.v126.23.1431.1431.

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Abstract Genomic instability is not only a hallmark of cancer, but potentially a primary mechanism for its occurrence. DNA repair mechanisms play a protective role during DNA damage induced by both normal metabolic activities and environmental factors such as reactive oxygen species (ROS), UV light and γ-irradiation. Genes related to DNA repair are usually considered as tumor suppressors. However, incomplete repair may induce severe genomic instability, leading eventually to transformation. Apurinic/apyrimidinic endonuclease 1 (APEX1), a gene involved in DNA repair with an important role in th
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10

Merk, Dennis, Johannes Ptok, Philipp Jakobs, et al. "Selenoprotein T Protects Endothelial Cells against Lipopolysaccharide-Induced Activation and Apoptosis." Antioxidants 10, no. 9 (2021): 1427. http://dx.doi.org/10.3390/antiox10091427.

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Sepsis is an exaggerated immune response upon infection with lipopolysaccharide (LPS) as the main causative agent. LPS-induced activation and apoptosis of endothelial cells (EC) can lead to organ dysfunction and finally organ failure. We previously demonstrated that the first twenty amino acids of the Apurinic/Apyrimidinic Endodeoxyribonuclease 1 (APEX1) are sufficient to inhibit EC apoptosis. To identify genes whose regulation by LPS is affected by this N-terminal APEX1 peptide, EC were transduced with an expression vector for the APEX1 peptide or an empty control vector and treated with LPS.
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11

Liu, Jiabin, Wei Jia, Rui-Xi Hua, et al. "APEX1 Polymorphisms and Neuroblastoma Risk in Chinese Children: A Three-Center Case-Control Study." Oxidative Medicine and Cellular Longevity 2019 (June 25, 2019): 1–8. http://dx.doi.org/10.1155/2019/5736175.

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Neuroblastoma is a life-threatening extracranial solid tumor, preferentially occurring in children. However, its etiology remains unclear. APEX1 is a critical gene in the base excision repair (BER) system responsible for maintaining genome stability. Given the potential effects of APEX1 polymorphisms on the ability of the DNA damage repair, many studies have investigated the association between these variants and susceptibility to several types of cancer but not neuroblastoma. Here, we conducted a three-center case-control study to evaluate the association between APEX1 polymorphisms (rs113040
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Sandoval-Carrillo, Ada, Edna Méndez-Hernández, Fernando Vazquez-Alaniz, et al. "Polymorphisms in DNA Repair Genes (APEX1, XPD, XRCC1 and XRCC3) and Risk of Preeclampsia in a Mexican Mestizo Population." International Journal of Molecular Sciences 15, no. 3 (2014): 4273–83. http://dx.doi.org/10.3390/ijms15034273.

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Variations in genes involved in DNA repair systems have been proposed as risk factors for the development of preeclampsia (PE). We conducted a case-control study to investigate the association of Human apurinic/apyrimidinic (AP) endonuclease (APEX1) Asp148Glu (rs1130409), Xeroderma Pigmentosum group D (XPD) Lys751Gln (rs13181), X-ray repair cross-complementing group 1 (XRCC) Arg399Gln (rs25487) and X-ray repair cross-complementing group 3 (XRCC3) Thr241Met (rs861539) polymorphisms with PE in a Mexican population. Samples of 202 cases and 350 controls were genotyped using RTPCR. Association ana
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13

Britt, Michael. "APEX1, a library of dynamic programming examples." ACM SIGCSE Bulletin 21, no. 1 (1989): 98–102. http://dx.doi.org/10.1145/65294.71196.

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Ding, Enmin, Jiadi Guo, Xin Ge, et al. "Analysis of Polymorphisms Associated with Base Excision Repair in Patients Susceptible and Resistant to Noise-Induced Hearing Loss." Disease Markers 2019 (November 14, 2019): 1–8. http://dx.doi.org/10.1155/2019/9327106.

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Objective. Noise-induced hearing loss (NIHL) is one of the most common occupational health risks in both developed and industrialized countries. It occurs as a result of interactions between genetic and environmental factors. Nevertheless, inherited genetic factors contributing to NIHL are not well understood. Therefore, we aim to investigate whether genetic mutations in three important base excision repair genes (OGG1, APEX1, and XRCC1) may influence susceptibility to NIHL. Methods. Three SNPs in OGG1, APEX1, and XRCC1 were genotyped from 1170 noise-exposed workers and were classified into 11
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15

Talluri, Srikanth, Jialan Shi, Mychell Neptune-Buon, et al. "A High Throughput Functional Screen Identifies a Novel Apex Inhibitor: Augments Cytotoxicity While Significantly Decreasing Genomic Evolution in Myeloma." Blood 136, Supplement 1 (2020): 10–11. http://dx.doi.org/10.1182/blood-2020-139945.

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Multiple myeloma (MM) is molecularly heterogenous disease with significant genomic instability. It carries number of mutations at diagnosis (median > 7000) and acquires additional changes overtime. With this background, we have evaluated the molecular intermediates of genomic instability in MM. Based on our large transcriptomic data we have identified apurinic/apyrimidinic deoxyribonuclease (APEX) as an important target whose elevated activity contributes to dysregulation of homologous recombination (HR) and genome stability in MM. Our investigation also demonstrates that transgenic ove
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HU, ZHAOHUI, XIANGJUN DING, YUYAO JI, XIAOHONG LIU, and ZHIWEN DING. "APEX1 protects against oxidative damage-induced cardiomyocyte apoptosis." BIOCELL 45, no. 3 (2021): 745–49. http://dx.doi.org/10.32604/biocell.2021.013293.

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Титов, Р. А., В. И. Минина, М. Л. Баканова, and Я. А. Савченко. "Polymorphic variants of DNA repair enzyme genes in the pathogenesis of lung cancer in women." Nauchno-prakticheskii zhurnal «Medicinskaia genetika», no. 6(215) (June 29, 2020): 86–87. http://dx.doi.org/10.25557/2073-7998.2020.06.86-87.

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Обследовано 540 жительниц Кемеровской области: 270 человек, первично обратившиеся для диагностики и лечения в Кемеровский областной онкологический диспансер и 268 человек - здоровые женщины доноры Кемеровского областного центра крови (группа сравнения). Цель: изучение роли полиморфизма генов репарации ДНК в формировании рака легкого у женщин. Типирование полиморфных вариантов генов APEX1 (rs1130409), XRCC1 (rs25489), hOGG1 (rs1052133), XPD (rs13181), XPG (rs17655), XPC (rs2228001), ADPRT (rs1136410), АТМ (rs18015), NBS1 (rs1805794) осуществляли методом аллель-специфической ПЦР. Стaтистическую
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Malyarchuk, Svitlana, Reneau Castore, and Lynn Harrison. "Apex1 can cleave complex clustered DNA lesions in cells." DNA Repair 8, no. 12 (2009): 1343–54. http://dx.doi.org/10.1016/j.dnarep.2009.08.008.

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Aloise, Débora de Almeida, Wendel Coura-Vital, Mariângela Carneiro, et al. "Association between ocular toxoplasmosis and APEX1 and MYD88 polymorphism." Acta Tropica 221 (September 2021): 106006. http://dx.doi.org/10.1016/j.actatropica.2021.106006.

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Desai, Ravi V., Xinyue Chen, Benjamin Martin, et al. "A DNA repair pathway can regulate transcriptional noise to promote cell fate transitions." Science 373, no. 6557 (2021): eabc6506. http://dx.doi.org/10.1126/science.abc6506.

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Stochastic fluctuations in gene expression (“noise”) are often considered detrimental, but fluctuations can also be exploited for benefit (e.g., dither). We show here that DNA base excision repair amplifies transcriptional noise to facilitate cellular reprogramming. Specifically, the DNA repair protein Apex1, which recognizes both naturally occurring and unnatural base modifications, amplifies expression noise while homeostatically maintaining mean expression levels. This amplified expression noise originates from shorter-duration, higher-intensity transcriptional bursts generated by Apex1-med
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Cao, Lei, Hongwei Cheng, Qiuxia Jiang, Hui Li, and Zhixian Wu. "APEX1 is a novel diagnostic and prognostic biomarker for hepatocellular carcinoma." Aging 12, no. 5 (2020): 4573–91. http://dx.doi.org/10.18632/aging.102913.

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Kim, Mi-Hwa, Hong-Beum Kim, Sang Pil Yoon, et al. "Colon cancer progression is driven by APEX1-mediated upregulation of Jagged." Journal of Clinical Investigation 123, no. 8 (2013): 3211–30. http://dx.doi.org/10.1172/jci65521.

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Dumitrache, Lavinia C., Mikio Shimada, Susanna M. Downing, et al. "Apurinic endonuclease-1 preserves neural genome integrity to maintain homeostasis and thermoregulation and prevent brain tumors." Proceedings of the National Academy of Sciences 115, no. 52 (2018): E12285—E12294. http://dx.doi.org/10.1073/pnas.1809682115.

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Frequent oxidative modification of the neural genome is a by-product of the high oxygen consumption of the nervous system. Rapid correction of oxidative DNA lesions is essential, as genome stability is a paramount determinant of neural homeostasis. Apurinic/apyrimidinic endonuclease 1 (APE1; also known as “APEX1” or “REF1”) is a key enzyme for the repair of oxidative DNA damage, although the specific role(s) for this enzyme in the development and maintenance of the nervous system is largely unknown. Here, using conditional inactivation of murine Ape1, we identify critical roles for this protei
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Wang, Yi, Craig C. Shupenko, Luisa F. Melo, and Phyllis R. Strauss. "DNA Repair Protein Involved in Heart and Blood Development." Molecular and Cellular Biology 26, no. 23 (2006): 9083–93. http://dx.doi.org/10.1128/mcb.01216-06.

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ABSTRACT Apurinic/apyrimidinic endonuclease 1, a key enzyme in repairing abasic sites in DNA, is an embryonic lethal in mice. We are examining its role in embryogenesis in zebra fish. Zebra fish contain two genomic copies (zfAPEX1a and zfAPEX1b) with identical coding sequences. zfAPEX1b lacks introns. Recombinant protein (ZAP1) is highly homologous with and has the same enzymatic properties as its human orthologue. ZAP1 is highly expressed throughout development. Embryos microinjected with morpholino oligonucleotide (MO) targeting the translation start site die at approximately the midblastula
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Kim, Hong-Beum, Won Jin Cho, Nam Gyu Choi, et al. "Clinical implications of APEX1 and Jagged1 as chemoresistance factors in biliary tract cancer." Annals of Surgical Treatment and Research 92, no. 1 (2017): 15. http://dx.doi.org/10.4174/astr.2017.92.1.15.

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Coppedè, Fabio, Annalisa Lo Gerfo, Cecilia Carlesi, et al. "Lack of association between the APEX1 Asp148Glu polymorphism and sporadic amyotrophic lateral sclerosis." Neurobiology of Aging 31, no. 2 (2010): 353–55. http://dx.doi.org/10.1016/j.neurobiolaging.2008.03.018.

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Kim, Hyery, Heewon Seo, Yoomi Park, et al. "APEX1 Polymorphism and Mercaptopurine-Related Early Onset Neutropenia in Pediatric Acute Lymphoblastic Leukemia." Cancer Research and Treatment 50, no. 3 (2018): 823–34. http://dx.doi.org/10.4143/crt.2017.351.

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Costa, Ericka Francislaine Dias, Erika Stocco dos Santos, Vitor Teixeira Liutti, et al. "OGG1, APEX1 and XRCC1 polymorphisms in oropharyngeal squamous cell carcinoma risk and prognosis." Journal of Clinical Oncology 34, no. 15_suppl (2016): e17515-e17515. http://dx.doi.org/10.1200/jco.2016.34.15_suppl.e17515.

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Kuasne, H., I. S. Rodrigues, R. Losi-Guembarovski, et al. "Base excision repair genes XRCC1 and APEX1 and the risk for prostate cancer." Molecular Biology Reports 38, no. 3 (2010): 1585–91. http://dx.doi.org/10.1007/s11033-010-0267-z.

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Milić, Mirta, Ružica Rozgaj, Vilena Kašuba, et al. "Polymorphisms in DNA repair genes: link with biomarkers of the CBMN cytome assay in hospital workers chronically exposed to low doses of ionising radiation / Polimorfizmi u genima za popravak DNA: poveznica s biomarkerima mikronukleus-testa u medicinskih radnika kronično izloženih niskim dozama ionizirajućeg zračenja." Archives of Industrial Hygiene and Toxicology 66, no. 2 (2015): 109–20. http://dx.doi.org/10.1515/aiht-2015-66-2655.

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Abstract Individual sensitivity to ionising radiation (IR) is the result of interaction between exposure, DNA damage, and its repair, which is why polymorphisms in DNA repair genes could play an important role. We examined the association between DNA damage, expressed as micronuclei (MNi), nuclear buds (NBs), and nucleoplasmic bridges (NPBs) and single nucleotide polymorphisms in selected DNA repair genes (APE1, hOGG1, XRCC1, XRCC3, XPD, PARP1, MGMT genes; representative of the different DNA repair pathways operating in mammals) in 77 hospital workers chronically exposed to low doses of IR, an
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Ali, Kashif, Ishrat Mahjabeen, Maimoona Sabir, et al. "Germline Variations of Apurinic/Apyrimidinic Endonuclease 1 (APEX1) Detected in Female Breast Cancer Patients." Asian Pacific Journal of Cancer Prevention 15, no. 18 (2014): 7589–95. http://dx.doi.org/10.7314/apjcp.2014.15.18.7589.

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Balasubramanian, Pavithra K., Anand Balupuri, and Seung Joo Cho. "Structural insights into the ligand-binding hot spots of APEX1: an in silico analysis." Medicinal Chemistry Research 24, no. 8 (2015): 3242–46. http://dx.doi.org/10.1007/s00044-015-1379-8.

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Laudencia-Chingcuanco, Debbie, and Sarah Hake. "The indeterminate floral apex1 gene regulates meristem determinacy and identity in the maize inflorescence." Development 129, no. 11 (2002): 2629–38. http://dx.doi.org/10.1242/dev.129.11.2629.

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Meristems may be determinate or indeterminate. In maize, the indeterminate inflorescence meristem produces three types of determinate meristems: spikelet pair, spikelet and floral meristems. These meristems are defined by their position and their products. We have discovered a gene in maize, indeterminate floral apex1 (ifa1) that regulates meristem determinacy. The defect found in ifa1 mutants is specific to meristems and does not affect lateral organs. In ifa1 mutants, the determinate meristems become less determinate. The spikelet pair meristem initiates more than a pair of spikelets and the
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Saad, Ahmad M., Ahmed E. S. Abdel‐Megied, Rizk A. Elbaz, Sobhy E. Hassab El‐Nabi, and Rami M. Elshazli. "Genetic variants of APEX1 p.Asp148Glu and XRCC1 p.Gln399Arg with the susceptibility of hepatocellular carcinoma." Journal of Medical Virology 93, no. 11 (2021): 6278–91. http://dx.doi.org/10.1002/jmv.27217.

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KIM, HONG-BEUM, HYUN-JONG LIM, HEE-JEONG LEE, JUN HEE PARK, and SANG-GON PARK. "Evaluation and Clinical Significance of Jagged-1-activated Notch Signaling by APEX1 in Colorectal Cancer." Anticancer Research 39, no. 11 (2019): 6097–105. http://dx.doi.org/10.21873/anticanres.13817.

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Torres-Ortiz⁎, Ceidy, Christi A. Walter, Sylvette Ayala-Torres, and Carlos A. Torres-Ramos. "Mitochondrial DNA damage increases in an age-dependent manner in liver from APEX1 haploinsufficient mice." Mitochondrion 11, no. 4 (2011): 659–60. http://dx.doi.org/10.1016/j.mito.2011.03.074.

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McManus, Frances, William Sands, Louise Diver, et al. "APEX1 Regulation of Aldosterone Synthase Gene Transcription Is Disrupted by a Common Polymorphism in Humans." Circulation Research 111, no. 2 (2012): 212–19. http://dx.doi.org/10.1161/circresaha.111.262931.

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Vogel, Kristine S., Marissa Perez, Jamila R. Momand, et al. "Age-related instability in spermatogenic cell nuclear and mitochondrial DNA obtained from Apex1 heterozygous mice." Molecular Reproduction and Development 78, no. 12 (2011): 906–19. http://dx.doi.org/10.1002/mrd.21374.

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Peng, Qiliu, Yu Lu, Xianjun Lao, et al. "Association between OGG1 Ser326Cys and APEX1 Asp148Glu polymorphisms and breast cancer risk: a meta-analysis." Diagnostic Pathology 9, no. 1 (2014): 108. http://dx.doi.org/10.1186/1746-1596-9-108.

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Yang, Jilong, Da Yang, David Cogdell, et al. "APEX1 Gene Amplification and Its Protein Overexpression in Osteosarcoma: Correlation with Recurrence, Metastasis, and Survival." Technology in Cancer Research & Treatment 9, no. 2 (2010): 161–69. http://dx.doi.org/10.1177/153303461000900205.

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KIM, HONG-BEUM, HEE-JEONG LEE, GEE-BEUM KIM, HYUN-JONG LIM, JUN HEE PARK, and SANG-GON PARK. "Clinical Significance of Jagged-1 Activated by APEX1 as a Chemoresistance Factor in Advanced Gastric Cancer." Anticancer Research 40, no. 4 (2020): 1897–904. http://dx.doi.org/10.21873/anticanres.14144.

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Kasahara, Mayumi, Kayo Osawa, Kana Yoshida, et al. "Association of MUTYH Gln324His and APEX1 Asp148Glu with colorectal cancer and smoking in a Japanese population." Journal of Experimental & Clinical Cancer Research 27, no. 1 (2008): 49. http://dx.doi.org/10.1186/1756-9966-27-49.

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Mahjabeen, Ishrat, Ruqia Mehmood Baig, Maimoona Sabir, and Mahmood Akhtar Kayani. "Genetic and expressional variations of APEX1 are associated with increased risk of head and neck cancer." Mutagenesis 28, no. 2 (2013): 213–18. http://dx.doi.org/10.1093/mutage/ges074.

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Cabral, B. B., F. V. Riva, Í. Rabinovich, M. Olandoski, L. Noronha, and V. S. Sotomaior. "Parkin, APEX1 and BCL2L1 tissue expression in southern Brazilian patients with different breast cancer molecular subtypes." Annals of Oncology 30 (October 2019): v22. http://dx.doi.org/10.1093/annonc/mdz238.077.

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Chang, Wen-Shin. "The Role of APEX1/Ref-1 (Apurinic/Apyrimidic Endonuclease DNA-Repair Gene) in Renal Cell Carcinoma." Adaptive Medicine 4, no. 4 (2012): 216–23. http://dx.doi.org/10.4247/am.2012.abc038.

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Wei, Wu, Xiao-Feng He, Jiang-Bo Qin, et al. "Association between the OGG1 Ser326Cys and APEX1 Asp148Glu polymorphisms and lung cancer risk: a meta-analysis." Molecular Biology Reports 39, no. 12 (2012): 11249–62. http://dx.doi.org/10.1007/s11033-012-2035-8.

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Chen, Yang, Jie Li, and Zengnan Mo. "Association between the APEX1 Asp148Glu polymorphism and prostate cancer, especially among Asians: a new evidence-based analysis." Oncotarget 7, no. 32 (2016): 52530–40. http://dx.doi.org/10.18632/oncotarget.9693.

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Lee, Jae Min, Ye Jee Shim, Do-Hoon Kim, Nani Jung, and Jung-Sook Ha. "The Effect of NUDT15, TPMT, APEX1, and ITPA Genetic Variations on Mercaptopurine Treatment of Pediatric Acute Lymphoblastic Leukemia." Children 8, no. 3 (2021): 224. http://dx.doi.org/10.3390/children8030224.

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Abstract:
Mercaptopurine (MP) is a commonly used maintenance regimen for childhood acute lymphoblastic leukemia (ALL). However, 6-MP has a narrow therapeutic index, which causes dose-limiting toxicities in hematopoietic tissues. Recent studies reported several candidate pharmacogenetic markers such as TPMT, NUDT15, ITPA, and APEX1, which predict the possibility of 6-MP related toxicities. The aim of this study is to evaluate the effect of major variants of these genes on 6-MP intolerances and toxicities in pediatric acute lymphoblastic leukemia (ALL) patients. A total of 83 pediatric ALL patients were i
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Ataya, Farid Shokry, Dalia Fouad, Ajamaluddin Malik, and Hesham Mahmoud Saeed. "Molecular Cloning and 3D Structure Modeling of APEX1, DNA Base Excision Repair Enzyme from the Camel, Camelus dromedarius." International Journal of Molecular Sciences 13, no. 7 (2012): 8578–96. http://dx.doi.org/10.3390/ijms13078578.

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Tominaga, Y. "MUTYH prevents OGG1 or APEX1 from inappropriately processing its substrate or reaction product with its C-terminal domain." Nucleic Acids Research 32, no. 10 (2004): 3198–211. http://dx.doi.org/10.1093/nar/gkh642.

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