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  1. Article: Cell cycle proteins in normal and chemically induced abnormal secondary palate development: a review.

    Dhulipala, Vamsidhara C / Welshons, Wade V / Reddy, Chada S

    Human & experimental toxicology

    2006  Volume 25, Issue 11, Page(s) 675–682

    Abstract: Cell cycle progression and thus proper cell number is essential for normal development of organs and organisms. Craniofacial tissues including the secondary palate are vulnerable to disruption of cell cycle progression and proliferation by many chemicals ...

    Abstract Cell cycle progression and thus proper cell number is essential for normal development of organs and organisms. Craniofacial tissues including the secondary palate are vulnerable to disruption of cell cycle progression and proliferation by many chemicals including mycotoxin, secalonic acid D (SAD), glucocorticoids, retinoic acid and 2,3,7,8-tetrachlorodibenzodioxin. Induction of cleft palate (CP) by SAD in mice occurs from a reduction in the size of developing palatal shelves. This is associated with an inhibition of proliferation of murine and human embryonic palatal mesenchymal (MEPM and HEPM) cells as well as a G1/S block of cell cycle. In murine embryonic palates and HEPM cells, SAD inhibited G1/S-phase-specific cyclin-dependent kinase (CDK)2 activity, reduced the level of cyclin E and increased the level of the CDK2 inhibitor, p21. These results, together with those from other laboratories, suggest that common cell cycle protein targets (biomarkers), relevant to the pathogenesis of CP by multiple chemical exposures, that can form the basis for the diagnosis and the development of preventive strategies, are likely to exist.
    MeSH term(s) Abnormalities, Drug-Induced/metabolism ; Animals ; Cell Cycle Proteins/metabolism ; Cleft Palate/etiology ; Cleft Palate/metabolism ; Embryonic Development/drug effects ; Embryonic Development/physiology ; Humans ; Palate/abnormalities ; Palate/embryology ; Palate/metabolism ; Teratogens/toxicity
    Chemical Substances Cell Cycle Proteins ; Teratogens
    Language English
    Publishing date 2006-11
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1027454-6
    ISSN 1477-0903 ; 0960-3271 ; 0144-5952
    ISSN (online) 1477-0903
    ISSN 0960-3271 ; 0144-5952
    DOI 10.1177/0960327106070848
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1697: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Role of p21 and cyclin E in normal and secalonic acid D-inhibited proliferation of human embryonic palatal mesenchymal cells.

    Dhulipala, Vamsidhara C / Maddali, Kamala K / Ray, Bimal K / Welshons, Wade V / Reddy, Chada S

    Human & experimental toxicology

    2011  Volume 30, Issue 9, Page(s) 1222–1232

    Abstract: Secalonic acid D (SAD), a cleft palate-inducing teratogen, has been shown to inhibit proliferation/cell cycle progression in association with alteration in the levels of cell cycle regulators, p21 and cyclin E. These studies were conducted to test the ... ...

    Abstract Secalonic acid D (SAD), a cleft palate-inducing teratogen, has been shown to inhibit proliferation/cell cycle progression in association with alteration in the levels of cell cycle regulators, p21 and cyclin E. These studies were conducted to test the hypotheses that p21 and cyclin E play an important functional role in normal human embryonic palatal mesenchymal (HEPM) cell cycle and that their up- and down-regulation, respectively, by SAD is functionally significant to its cell cycle block. Using small interfering RNA (siRNA) to silence p21 gene and transient transfection to overexpress cyclin E in control & SAD-treated HEPM cells, cell proliferation was assessed using a combination of cell numbers, thymidine uptake, CDK2 activity and Ki-67 expression. The results showed that silencing of p21 gene, although increased cell proliferation/numbers and CDK2 activity in normal HEPM cells, failed to counteract SAD-induced anti-proliferative effect despite inducing partial recovery of CDK2 activity. Similar effects were apparent with cyclin E overexpression. It is concluded that p21 and cyclin E are important for normal HEPM cell proliferation. However, SAD-induced deregulation of either protein, singly, may not be sufficient to induce anti-proliferative effect. Involvement of other cell cycle proteins such as cyclin D1 or of multiple proteins in SAD-induced cell cycle block needs to be examined.
    MeSH term(s) Cell Culture Techniques ; Cell Cycle/drug effects ; Cell Line ; Cell Proliferation/drug effects ; Cyclin E/genetics ; Cyclin E/metabolism ; Cyclin E/physiology ; Cyclin-Dependent Kinase Inhibitor p21/genetics ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Cyclin-Dependent Kinase Inhibitor p21/physiology ; Gene Silencing ; Humans ; Immunoblotting ; Mesoderm/cytology ; Mesoderm/drug effects ; Mesoderm/metabolism ; Palate/cytology ; Palate/drug effects ; Palate/embryology ; Palate/metabolism ; RNA, Small Interfering/pharmacology ; Xanthones/pharmacology
    Chemical Substances CDKN1A protein, human ; Cyclin E ; Cyclin-Dependent Kinase Inhibitor p21 ; RNA, Small Interfering ; Xanthones ; secalonic acid (56283-72-8)
    Language English
    Publishing date 2011-09
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1027454-6
    ISSN 1477-0903 ; 0144-5952 ; 0960-3271
    ISSN (online) 1477-0903
    ISSN 0144-5952 ; 0960-3271
    DOI 10.1177/0960327110387238
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1697: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article: Mechanism of secalonic acid D-induced inhibition of transcription factor binding to cyclic AMP response element in the developing murine palate.

    Hanumegowda, Umesh M / Dhulipala, Vamsidhara C / Reddy, Chada S

    Toxicological sciences : an official journal of the Society of Toxicology

    2002  Volume 70, Issue 1, Page(s) 55–62

    Abstract: Regulation of gene expression via the protein kinase A (PKA) pathway is mediated through Ser133 phosphorylation of the transcription factor (TF), cAMP response element (CRE) binding protein (CREB). Secalonic acid D (SAD), a mycotoxin causing cleft palate ...

    Abstract Regulation of gene expression via the protein kinase A (PKA) pathway is mediated through Ser133 phosphorylation of the transcription factor (TF), cAMP response element (CRE) binding protein (CREB). Secalonic acid D (SAD), a mycotoxin causing cleft palate (CP), induces phosphorylation of palatal CREB in vivo. SAD-induced increase in phosphoCREB (pCREB), however, is associated with decreased binding of TF to CRE in vivo. Mechanism(s) involved in these two effects of SAD were studied using palatal nuclear extracts (PNE). Stimulation of CREB phosphorylation by SAD was confirmed in vitro in both cell culture and cell-free systems, and this phosphorylation was not altered by currently known CREB kinase (PKA, CaMK, MEK, p38MAPK, PKC) or phosphatase inhibitors. SAD-induced increase in pCREB, however, was associated with decreased TF binding to CRE in vitro. Two-dimensional gel analysis ruled out additional inhibitory phosphorylations. Addition of SAD to PNE following an increase in PKA-phosphorylated CREB resulted in reduced TF binding to CRE. Further, SAD was shown to bind directly to phosphorylated nuclear proteins (pCREB) with greater affinity. In addition, the inhibitory effect of SAD occurred with CRE of proliferating cell nuclear antigen (PCNA) gene. These studies confirm that stimulation of CREB phosphorylation by SAD does not involve sites other than Ser133 and is mediated by a novel kinase. They also indicate that SAD directly binds to CREB to inhibit its binding to CRE of genes such as PCNA. This effect could lead to reduced palatal mesenchymal cell number, smaller palatal shelf, and thus CP.
    MeSH term(s) Animals ; CREB-Binding Protein ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/genetics ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Dose-Response Relationship, Drug ; Female ; Gene Expression Regulation, Developmental/genetics ; Male ; Mice ; Mice, Inbred Strains ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Palate/abnormalities ; Palate/embryology ; Palate/metabolism ; Phosphorylation ; Proliferating Cell Nuclear Antigen/metabolism ; Protein Binding/drug effects ; Signal Transduction/genetics ; Teratogens/pharmacology ; Teratogens/toxicity ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Xanthenes/pharmacology ; Xanthenes/toxicity ; Xanthones
    Chemical Substances Cyclic AMP Response Element-Binding Protein ; Nuclear Proteins ; Proliferating Cell Nuclear Antigen ; Teratogens ; Trans-Activators ; Transcription Factors ; Xanthenes ; Xanthones ; secalonic acid (56283-72-8) ; CREB-Binding Protein (EC 2.3.1.48) ; Crebbp protein, mouse (EC 2.3.1.48) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11)
    Language English
    Publishing date 2002-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1420885-4
    ISSN 1096-0929 ; 1096-6080
    ISSN (online) 1096-0929
    ISSN 1096-6080
    DOI 10.1093/toxsci/70.1.55
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1709: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  4. Article: Relevance of the palatal protein kinase A pathway to the pathogenesis of cleft palate by secalonic acid D in mice.

    Dhulipala, Vamsidhara C / Hanumegowda, Umesh M / Balasubramanian, Ganesh / Reddy, Chada S

    Toxicology and applied pharmacology

    2004  Volume 194, Issue 3, Page(s) 270–279

    Abstract: Secalonic acid-D (SAD) is a teratogenic mycotoxin inducing cleft palate (CP) in the offspring of the exposed mice by reducing palatal shelf size secondary to reduced proliferation of the palatal mesenchymal (PM) cells. Co-administration of ... ...

    Abstract Secalonic acid-D (SAD) is a teratogenic mycotoxin inducing cleft palate (CP) in the offspring of the exposed mice by reducing palatal shelf size secondary to reduced proliferation of the palatal mesenchymal (PM) cells. Co-administration of dimethylsulfoxide (DMSO) reversed the CP-inducing effect of SAD. Although SAD has been shown to affect both protein kinases A (PKA) and C (PKC) pathways, the relevance of each of these pathways to its CP induction is unknown. The present studies were designed to test the hypothesis that the protective effect of DMSO is mediated by its specific reversal of the effect(s) of SAD on one of these two pathways using ELISA-based activity assays, Western blot analysis, electrophoretic mobility shift assays (EMSA), and murine embryonic PM (MEPM) cell growth in culture. Within the PKA pathway, SAD inhibited the activity of the catalytic subunit of PKA and its migration into the nucleus, elevated phosphorylated cyclic AMP (cAMP) response element (CRE)-binding protein (pCREB) level, and reduced the binding of CREB to CRE. In the PKC pathway, SAD reduced the activity of PKC and the binding of transcription factors (TF) to 12-O-tetradecanoate-13 phorbol acetate-response element (TRE). SAD also inhibited MEPM cell growth and the expression of the CRE- and TRE-containing gene, proliferating cell nuclear antigen (PCNA). Reversal, by DMSO, of the effects of SAD on MEPM cell growth, on PCNA expression and on all components of the PKA, but not of PKC, pathway suggests that the perturbation of the PKA pathway by SAD is relevant to its induction of CP in mice.
    MeSH term(s) Animals ; Blotting, Western ; Catalysis ; Cell Division/drug effects ; Cell Nucleus/metabolism ; Cleft Palate/chemically induced ; Cleft Palate/enzymology ; Cleft Palate/pathology ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors ; Cyclic AMP-Dependent Protein Kinases/physiology ; Dimethyl Sulfoxide/pharmacology ; Dose-Response Relationship, Drug ; Electrophoretic Mobility Shift Assay ; Enzyme Inhibitors/pharmacology ; Female ; Gene Expression/drug effects ; Mice ; Palate/cytology ; Palate/enzymology ; Phosphorylation ; Pregnancy ; Proliferating Cell Nuclear Antigen/biosynthesis ; Proliferating Cell Nuclear Antigen/genetics ; Protein Kinase C/antagonists & inhibitors ; Protein Kinase C/metabolism ; Response Elements/genetics ; Signal Transduction/drug effects ; Teratogens/toxicity ; Transcription Factors/metabolism ; Xanthones/antagonists & inhibitors ; Xanthones/metabolism ; Xanthones/toxicity
    Chemical Substances Cyclic AMP Response Element-Binding Protein ; Enzyme Inhibitors ; Proliferating Cell Nuclear Antigen ; Teratogens ; Transcription Factors ; Xanthones ; secalonic acid (56283-72-8) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; Protein Kinase C (EC 2.7.11.13) ; Dimethyl Sulfoxide (YOW8V9698H)
    Language English
    Publishing date 2004-02-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 204477-8
    ISSN 1096-0333 ; 0041-008X
    ISSN (online) 1096-0333
    ISSN 0041-008X
    DOI 10.1016/j.taap.2003.09.014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 14: Show issues Location:
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