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  1. AU="Davis, Anthony J"
  2. AU=Schulte-Hillen Catrin
  3. AU="Fernandes, Marcos Rassi"
  4. AU="H.Qi, "
  5. AU="Reza Maroofian"
  6. AU="Chien, Chia-Yu"
  7. AU="Ward, John W" AU="Ward, John W"
  8. AU="Peña-Santiago, Reyes"
  9. AU="Ottens, R S"
  10. AU=Sharma S K AU=Sharma S K
  11. AU="Schuchard, Karl G"
  12. AU="Lawton, Michael T."
  13. AU="Marazuela, Rosario"
  14. AU="Gandini, O"
  15. AU="Mahadevan, L"
  16. AU="Hsiao, Chen-Tsung"
  17. AU=Kyriazopoulou Evdoxia AU=Kyriazopoulou Evdoxia
  18. AU="Kalezić, Tanja"
  19. AU="Ng, Andrew A"
  20. AU="Maeda, Shunta"
  21. AU="Ma, Yongjie"
  22. AU="Fukamizu, Akiyoshi"
  23. AU="Maclean, Ilya M. D."
  24. AU=Alpers Charles E
  25. AU=Lippi Giuseppe
  26. AU="Ricci, Giampietro"
  27. AU="Marshall, Andrew"
  28. AU="Zhen-dong HUA"
  29. AU="John P. Thomas"
  30. AU="Airton Massaro"
  31. AU="Isabelle Hautefort"

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  1. Artikel: Human RecQ Helicases in DNA Double-Strand Break Repair.

    Lu, Huiming / Davis, Anthony J

    Frontiers in cell and developmental biology

    2021  Band 9, Seite(n) 640755

    Abstract: RecQ DNA helicases are a conserved protein family found in bacteria, fungus, plants, and animals. These helicases play important roles in multiple cellular functions, including DNA replication, transcription, DNA repair, and telomere maintenance. Humans ... ...

    Abstract RecQ DNA helicases are a conserved protein family found in bacteria, fungus, plants, and animals. These helicases play important roles in multiple cellular functions, including DNA replication, transcription, DNA repair, and telomere maintenance. Humans have five RecQ helicases: RECQL1, Bloom syndrome protein (BLM), Werner syndrome helicase (WRN), RECQL4, and RECQL5. Defects in BLM and WRN cause autosomal disorders: Bloom syndrome (BS) and Werner syndrome (WS), respectively. Mutations in RECQL4 are associated with three genetic disorders, Rothmund-Thomson syndrome (RTS), Baller-Gerold syndrome (BGS), and RAPADILINO syndrome. Although no genetic disorders have been reported due to loss of RECQL1 or RECQL5, dysfunction of either gene is associated with tumorigenesis. Multiple genetically independent pathways have evolved that mediate the repair of DNA double-strand break (DSB), and RecQ helicases play pivotal roles in each of them. The importance of DSB repair is supported by the observations that defective DSB repair can cause chromosomal aberrations, genomic instability, senescence, or cell death, which ultimately can lead to premature aging, neurodegeneration, or tumorigenesis. In this review, we will introduce the human RecQ helicase family, describe in detail their roles in DSB repair, and provide relevance between the dysfunction of RecQ helicases and human diseases.
    Sprache Englisch
    Erscheinungsdatum 2021-02-25
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2021.640755
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: The Cancer Testes Antigen, HORMAD1, is a Tumor-Specific Replication Fork Protection Factor.

    Herrera, Luis Reza / McGlynn, Kathleen / Gibbs, Zane A / Davis, Anthony J / Whitehurst, Angelique W

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Tumors frequently activate the expression of genes that are only otherwise required for meiosis. HORMAD1, which is essential for meiotic recombination in multiple species, is expressed in over 50% of human lung adenocarcinoma cells (LUAD). We previously ... ...

    Abstract Tumors frequently activate the expression of genes that are only otherwise required for meiosis. HORMAD1, which is essential for meiotic recombination in multiple species, is expressed in over 50% of human lung adenocarcinoma cells (LUAD). We previously found that HORMAD1 promotes DNA double strand break (DSB) repair in LUAD. Here, we report that HORMAD1 takes on an additional role in protecting genomic integrity. Specifically, we find HORMAD1 is critical for protecting stalled DNA replication forks in LUAD. Loss of HORMAD1 leads to nascent DNA degradation, an event which is mediated by the MRE11-DNA2-BLM pathway. Moreover, following exogenous induction of DNA replication stress, HORMAD1 deleted cells accumulate single stranded DNA (ssDNA). We find that these phenotypes are the result of a lack of RAD51 and BRCA2 loading onto stalled replication forks. Ultimately, loss of HORMAD1 leads to increased DSBs and chromosomal aberrations in response to replication stress. Collectively, our data support a model where HORMAD1 expression is selected to mitigate DNA replication stress, which would otherwise induce deleterious genomic instability.
    Sprache Englisch
    Erscheinungsdatum 2023-02-03
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2023.01.31.526348
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: DNA-PKcs-dependent phosphorylation of RECQL4 promotes NHEJ by stabilizing the NHEJ machinery at DNA double-strand breaks.

    Lu, Huiming / Guan, Junhong / Wang, Shih-Ya / Li, Guo-Min / Bohr, Vilhelm A / Davis, Anthony J

    Nucleic acids research

    2022  Band 50, Heft 10, Seite(n) 5635–5651

    Abstract: Non-homologous end joining (NHEJ) is the major pathway that mediates the repair of DNA double-strand breaks (DSBs) generated by ionizing radiation (IR). Previously, the DNA helicase RECQL4 was implicated in promoting NHEJ, but its role in the pathway ... ...

    Abstract Non-homologous end joining (NHEJ) is the major pathway that mediates the repair of DNA double-strand breaks (DSBs) generated by ionizing radiation (IR). Previously, the DNA helicase RECQL4 was implicated in promoting NHEJ, but its role in the pathway remains unresolved. In this study, we report that RECQL4 stabilizes the NHEJ machinery at DSBs to promote repair. Specifically, we find that RECQL4 interacts with the NHEJ core factor DNA-PKcs and the interaction is increased following IR. RECQL4 promotes DNA end bridging mediated by DNA-PKcs and Ku70/80 in vitro and the accumulation/retention of NHEJ factors at DSBs in vivo. Moreover, interaction between DNA-PKcs and the other core NHEJ proteins following IR treatment is attenuated in the absence of RECQL4. These data indicate that RECQL4 promotes the stabilization of the NHEJ factors at DSBs to support formation of the NHEJ long-range synaptic complex. In addition, we observed that the kinase activity of DNA-PKcs is required for accumulation of RECQL4 to DSBs and that DNA-PKcs phosphorylates RECQL4 at six serine/threonine residues. Blocking phosphorylation at these sites reduced the recruitment of RECQL4 to DSBs, attenuated the interaction between RECQL4 and NHEJ factors, destabilized interactions between the NHEJ machinery, and resulted in decreased NHEJ. Collectively, these data illustrate reciprocal regulation between RECQL4 and DNA-PKcs in NHEJ.
    Mesh-Begriff(e) DNA/genetics ; DNA/metabolism ; DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; DNA Repair ; DNA-Activated Protein Kinase/genetics ; DNA-Activated Protein Kinase/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Phosphorylation ; RecQ Helicases/genetics ; RecQ Helicases/metabolism
    Chemische Substanzen DNA-Binding Proteins ; DNA (9007-49-2) ; DNA-Activated Protein Kinase (EC 2.7.11.1) ; RecQ Helicases (EC 3.6.4.12)
    Sprache Englisch
    Erscheinungsdatum 2022-05-16
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 186809-3
    ISSN 1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
    ISSN (online) 1362-4962 ; 1362-4954
    ISSN 0301-5610 ; 0305-1048
    DOI 10.1093/nar/gkac375
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: The Role of the Core Non-Homologous End Joining Factors in Carcinogenesis and Cancer.

    Sishc, Brock J / Davis, Anthony J

    Cancers

    2017  Band 9, Heft 7

    Abstract: DNA double-strand breaks (DSBs) are deleterious DNA lesions that if left unrepaired or are misrepaired, potentially result in chromosomal aberrations, known drivers of carcinogenesis. Pathways that direct the repair of DSBs are traditionally believed to ... ...

    Abstract DNA double-strand breaks (DSBs) are deleterious DNA lesions that if left unrepaired or are misrepaired, potentially result in chromosomal aberrations, known drivers of carcinogenesis. Pathways that direct the repair of DSBs are traditionally believed to be guardians of the genome as they protect cells from genomic instability. The prominent DSB repair pathway in human cells is the non-homologous end joining (NHEJ) pathway, which mediates template-independent re-ligation of the broken DNA molecule and is active in all phases of the cell cycle. Its role as a guardian of the genome is supported by the fact that defects in NHEJ lead to increased sensitivity to agents that induce DSBs and an increased frequency of chromosomal aberrations. Conversely, evidence from tumors and tumor cell lines has emerged that NHEJ also promotes chromosomal aberrations and genomic instability, particularly in cells that have a defect in one of the other DSB repair pathways. Collectively, the data present a conundrum: how can a single pathway both suppress and promote carcinogenesis? In this review, we will examine NHEJ's role as both a guardian and a disruptor of the genome and explain how underlying genetic context not only dictates whether NHEJ promotes or suppresses carcinogenesis, but also how it alters the response of tumors to conventional therapeutics.
    Sprache Englisch
    Erscheinungsdatum 2017-07-06
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers9070081
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel: ATM phosphorylates the FATC domain of DNA-PK

    Lu, Huiming / Zhang, Qin / Laverty, Daniel J / Puncheon, Andrew C / Williams, Gareth J / Nagel, Zachary D / Chen, Benjamin Pc / Davis, Anthony J

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Ataxia-telangiectasia mutated (ATM) drives the DNA damage response via modulation of multiple signal transduction and DNA repair pathways. Previously, ATM activity was implicated in promoting the non-homologous end joining (NHEJ) pathway to repair a ... ...

    Abstract Ataxia-telangiectasia mutated (ATM) drives the DNA damage response via modulation of multiple signal transduction and DNA repair pathways. Previously, ATM activity was implicated in promoting the non-homologous end joining (NHEJ) pathway to repair a subset of DNA double strand breaks (DSBs), but how ATM performs this function is still unclear. In this study, we identified that ATM phosphorylates the DNA-dependent protein kinase catalytic subunit (DNA-PK
    Sprache Englisch
    Erscheinungsdatum 2023-02-02
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2023.02.02.526879
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: The cancer testes antigen, HORMAD1, limits genomic instability in cancer cells by protecting stalled replication forks.

    Herrera, Luis Reza / Johnson, Ronnesha A / McGlynn, Kathleen / Gibbs, Zane A / Davis, Anthony J / Whitehurst, Angelique W

    The Journal of biological chemistry

    2023  Band 299, Heft 11, Seite(n) 105348

    Abstract: Tumors anomalously induce the expression of meiotic genes, which are otherwise restricted only to developing gametes. If and how these aberrantly expressed meiotic proteins influence DNA metabolism is not clear, but could have important implications for ... ...

    Abstract Tumors anomalously induce the expression of meiotic genes, which are otherwise restricted only to developing gametes. If and how these aberrantly expressed meiotic proteins influence DNA metabolism is not clear, but could have important implications for how tumors acquire and mitigate genomic instability. HORMAD1 is a highly conserved meiotic protein that is frequently expressed in lung adenocarincoma where its expression correlates with reduced patient survival and increased mutation burden. Here, we find that HORMAD1 associates with the replisome and is critical for protecting stalled DNA replication forks. Loss of HORMAD1 leads to nascent DNA strand degradation, an event which is mediated by the MRE11-DNA2-BLM pathway. We find that these phenotypes are due to limited RAD51 loading onto stalled replication forks in the absence of HORMAD1. Ultimately, loss of HORMAD1 leads to increased DNA breaks and chromosomal defects, which is exacerbated dramatically by induction of replication stress. Tumor cells proliferate despite encountering chronic replication stress, placing them on the precipice of catastrophic genomic damage. Our data support the hypothesis that the aberrant expression of HORMAD1 is engaged to attenuate the accumulation of excessive DNA damage due to chronic replication stress, which may otherwise lead to accumulation of toxic levels of genomic instability.
    Mesh-Begriff(e) Humans ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; DNA ; DNA Replication ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Genomic Instability ; Neoplasms/genetics
    Chemische Substanzen Cell Cycle Proteins ; DNA (9007-49-2) ; DNA-Binding Proteins ; HORMAD1 protein, human
    Sprache Englisch
    Erscheinungsdatum 2023-10-12
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2023.105348
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: DNA-PKcs and ATM modulate mitochondrial ADP-ATP exchange as an oxidative stress checkpoint mechanism.

    Chen, Wei-Min / Chiang, Jui-Chung / Shang, Zengfu / Palchik, Guillermo / Newman, Ciara / Zhang, Yuanyuan / Davis, Anthony J / Lee, Hsinyu / Chen, Benjamin Pc

    The EMBO journal

    2023  Band 42, Heft 6, Seite(n) e112094

    Abstract: DNA-PKcs is a key regulator of DNA double-strand break repair. Apart from its canonical role in the DNA damage response, DNA-PKcs is involved in the cellular response to oxidative stress (OS), but its exact role remains unclear. Here, we report that DNA- ... ...

    Abstract DNA-PKcs is a key regulator of DNA double-strand break repair. Apart from its canonical role in the DNA damage response, DNA-PKcs is involved in the cellular response to oxidative stress (OS), but its exact role remains unclear. Here, we report that DNA-PKcs-deficient human cells display depolarized mitochondria membrane potential (MMP) and reoriented metabolism, supporting a role for DNA-PKcs in oxidative phosphorylation (OXPHOS). DNA-PKcs directly interacts with mitochondria proteins ANT2 and VDAC2, and formation of the DNA-PKcs/ANT2/VDAC2 (DAV) complex supports optimal exchange of ADP and ATP across mitochondrial membranes to energize the cell via OXPHOS and to maintain MMP. Moreover, we demonstrate that the DAV complex temporarily dissociates in response to oxidative stress to attenuate ADP-ATP exchange, a rate-limiting step for OXPHOS. Finally, we found that dissociation of the DAV complex is mediated by phosphorylation of DNA-PKcs at its Thr2609 cluster by ATM kinase. Based on these findings, we propose that the coordination between the DAV complex and ATM serves as a novel oxidative stress checkpoint to decrease ROS production from mitochondrial OXPHOS and to hasten cellular recovery from OS.
    Mesh-Begriff(e) Humans ; Adenosine Triphosphate/metabolism ; Ataxia Telangiectasia Mutated Proteins/genetics ; Ataxia Telangiectasia Mutated Proteins/metabolism ; DNA/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Mitochondria/metabolism ; Oxidative Stress ; Phosphorylation
    Chemische Substanzen Adenosine Triphosphate (8L70Q75FXE) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; ATM protein, human (EC 2.7.11.1) ; DNA (9007-49-2) ; DNA-Binding Proteins
    Sprache Englisch
    Erscheinungsdatum 2023-02-02
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 586044-1
    ISSN 1460-2075 ; 0261-4189
    ISSN (online) 1460-2075
    ISSN 0261-4189
    DOI 10.15252/embj.2022112094
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel: BUB1 regulates non-homologous end joining pathway to mediate radioresistance in triple-negative breast cancer.

    Sriramulu, Sushmitha / Thoidingjam, Shivani / Chen, Wei-Min / Hassan, Oudai / Siddiqui, Farzan / Brown, Stephen L / Movsas, Benjamin / Green, Michael D / Davis, Anthony J / Speers, Corey / Walker, Eleanor / Nyati, Shyam

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Background: Triple-negative breast cancer (TNBC) is a highly aggressive form of breast cancer subtype often treated with radiotherapy (RT). Due to its intrinsic heterogeneity and lack of effective targets, it is crucial to identify novel molecular ... ...

    Abstract Background: Triple-negative breast cancer (TNBC) is a highly aggressive form of breast cancer subtype often treated with radiotherapy (RT). Due to its intrinsic heterogeneity and lack of effective targets, it is crucial to identify novel molecular targets that would increase RT efficacy. Here we demonstrate the role of BUB1 (cell cycle Ser/Thr kinase) in TNBC radioresistance and offer a novel strategy to improve TNBC treatment.
    Methods: Gene expression analysis was performed to look at genes upregulated in TNBC patient samples compared to other subtypes. Cell proliferation and clonogenic survivals assays determined the IC
    Results: BUB1 is overexpressed in BC and its expression is considerably elevated in TNBC with poor survival outcomes. Pharmacological or genomic ablation of BUB1 sensitized multiple TNBC cell lines to cell killing by radiation, although breast epithelial cells showed no radiosensitization with BUB1 inhibition. Kinase function of BUB1 is mainly accountable for this radiosensitization phenotype. BUB1 ablation also led to radiosensitization in TNBC tumor xenografts with significantly increased tumor growth delay and overall survival. Mechanistically, BUB1 ablation inhibited the repair of radiation-induced DNA double strand breaks (DSBs). BUB1 ablation stabilized phospho-DNAPKcs (S2056) following RT such that half-lives could not be estimated. In contrast, RT alone caused BUB1 stabilization, but pre-treatment with BUB1 inhibitor prevented stabilization (t
    Conclusions: BUB1 ablation sensitizes TNBC cell lines and xenografts to RT and BUB1 mediated radiosensitization may occur through NHEJ. Together, these results highlight BUB1 as a novel molecular target for radiosensitization in women with TNBC.
    Sprache Englisch
    Erscheinungsdatum 2024-05-10
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2024.05.07.592812
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Unsolved mystery: the role of BRCA1 in DNA end-joining.

    Saha, Janapriya / Davis, Anthony J

    Journal of radiation research

    2016  Band 57 Suppl 1, Seite(n) i18–i24

    Abstract: Heritable mutations in the tumor suppressor gene BRCA1 increase a woman's lifetime risk of developing breast and ovarian cancer. BRCA1's tumor suppressor function is directly linked to its myriad of functions in the cellular response to DNA double-strand ...

    Abstract Heritable mutations in the tumor suppressor gene BRCA1 increase a woman's lifetime risk of developing breast and ovarian cancer. BRCA1's tumor suppressor function is directly linked to its myriad of functions in the cellular response to DNA double-strand breaks (DSBs). BRCA1 interacts with an extensive array of DNA damage responsive proteins and plays important roles in DSB repair, mediated by the homologous recombination pathway, and in the activation of cell cycle checkpoints. However, the role of BRCA1 in the other two DSB repair pathways, classical non-homologous end-joining (C-NHEJ) and alternative NHEJ (A-NHEJ), remains unclear. In this review, we will discuss the current literature on BRCA1's potential role(s) in modulating both C-NHEJ and A-NHEJ. We also present a model showing that BRCA1 contributes to genomic maintenance by promoting precise DNA repair across all cell cycle phases via the direct modulation of DNA end-joining.
    Mesh-Begriff(e) Animals ; BRCA1 Protein/metabolism ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Cycle ; DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; Female ; Humans ; Models, Biological
    Chemische Substanzen BRCA1 Protein
    Sprache Englisch
    Erscheinungsdatum 2016-08
    Erscheinungsland England
    Dokumenttyp Journal Article ; Review
    ISSN 1349-9157
    ISSN (online) 1349-9157
    DOI 10.1093/jrr/rrw032
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  10. Artikel ; Online: Investigation of stillbirths, perinatal mortality and weakness in beef calves with low-selenium whole blood concentrations.

    Davis, Anthony J / Myburgh, Jan G

    Journal of the South African Veterinary Association

    2016  Band 87, Heft 1, Seite(n) e1–6

    Abstract: In this on-farm investigation, we report on stillbirths, weakness and perinatal mortality seen in calves on a commercial beef farm in the Roossenekal area, Mpumalanga province, South Africa. Post-mortem examination of these calves and histopathological ... ...

    Abstract In this on-farm investigation, we report on stillbirths, weakness and perinatal mortality seen in calves on a commercial beef farm in the Roossenekal area, Mpumalanga province, South Africa. Post-mortem examination of these calves and histopathological examination of organ and tissue samples did not indicate an infectious aetiology. Affected calves had marginal to deficient whole blood selenium concentrations. Whole blood samples collected from adult cattle on this farm and five neighbouring farms were deficient in selenium. The potential contributions of other minerals to the symptoms seen are a subject of ongoing investigation, but selenium deficiency was marked in this herd and required urgent correction. Methods to correct the deficiency included the use of injectable products, and an oral selenium supplement chelated to methionine. Selenium availability to plants is primarily determined by the selenium content of the parent bedrock, the presence of other minerals and the pH of the soil. The apparent sudden onset of this problem implicates a soil factor as being responsible for reducing selenium's bioavailability in this area. Selenium deficiency can have a significant impact on human health. HIV and/or AIDS, various forms of cancer and several specific clinical syndromes are associated with selenium deficiency in humans, and the impact on human health in this area also requires further investigation.
    Mesh-Begriff(e) Agriculture ; Animals ; Animals, Newborn/blood ; Cattle ; Cattle Diseases/blood ; Cattle Diseases/congenital ; Female ; Muscle Weakness/veterinary ; Selenium/blood ; Selenium/deficiency ; Sheep ; Sheep Diseases/blood ; Sheep Diseases/congenital ; Stillbirth/veterinary
    Chemische Substanzen Selenium (H6241UJ22B)
    Sprache Englisch
    Erscheinungsdatum 2016-07-15
    Erscheinungsland South Africa
    Dokumenttyp Case Reports ; Journal Article
    ZDB-ID 188571-6
    ISSN 2224-9435 ; 1019-9128 ; 0301-0732 ; 0038-2809
    ISSN (online) 2224-9435
    ISSN 1019-9128 ; 0301-0732 ; 0038-2809
    DOI 10.4102/jsava.v87i1.1336
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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