LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 16

Search options

  1. Article ; Online: The TRRAP transcription cofactor represses interferon-stimulated genes in colorectal cancer cells.

    Detilleux, Dylane / Raynaud, Peggy / Pradet-Balade, Berengere / Helmlinger, Dominique

    eLife

    2022  Volume 11

    Abstract: Transcription is essential for cells to respond to signaling cues and involves factors with multiple distinct activities. One such factor, TRRAP, functions as part of two large complexes, SAGA and TIP60, which have crucial roles during transcription ... ...

    Abstract Transcription is essential for cells to respond to signaling cues and involves factors with multiple distinct activities. One such factor, TRRAP, functions as part of two large complexes, SAGA and TIP60, which have crucial roles during transcription activation. Structurally, TRRAP belongs to the phosphoinositide 3 kinase-related kinases (PIKK) family but is the only member classified as a pseudokinase. Recent studies established that a dedicated HSP90 co-chaperone, the triple T (TTT) complex, is essential for PIKK stabilization and activity. Here, using endogenous auxin-inducible degron alleles, we show that the TTT subunit TELO2 promotes TRRAP assembly into SAGA and TIP60 in human colorectal cancer cells (CRCs). Transcriptomic analysis revealed that TELO2 contributes to TRRAP regulatory roles in CRC cells, most notably of MYC target genes. Surprisingly, TELO2 and TRRAP depletion also induced the expression of type I interferon genes. Using a combination of nascent RNA, antibody-targeted chromatin profiling (CUT&RUN), ChIP, and kinetic analyses, we propose a model by which TRRAP directly represses the transcription of
    MeSH term(s) Colorectal Neoplasms/genetics ; Histone Acetyltransferases/metabolism ; Humans ; Interferons ; Phosphatidylinositol 3-Kinases ; Transcription Factors/metabolism
    Chemical Substances Transcription Factors ; Interferons (9008-11-1) ; Histone Acetyltransferases (EC 2.3.1.48)
    Language English
    Publishing date 2022-03-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.69705
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article ; Online: The atypical RhoU/Wrch1 Rho GTPase controls cell proliferation and apoptosis in the gut epithelium.

    Slaymi, Chaker / Vignal, Emmanuel / Crès, Gaëlle / Roux, Pierre / Blangy, Anne / Raynaud, Peggy / Fort, Philippe

    Biology of the cell

    2019  Volume 111, Issue 5, Page(s) 121–141

    Abstract: Background: The mammalian gut epithelium displays among the highest rates of self-renewal, with a turnover time of less than 5 days. Renewal involves concerted proliferation at the bottom of the crypt, migration and differentiation along the crypt- ... ...

    Abstract Background: The mammalian gut epithelium displays among the highest rates of self-renewal, with a turnover time of less than 5 days. Renewal involves concerted proliferation at the bottom of the crypt, migration and differentiation along the crypt-villus axis and anoïkis/shedding in the luminal epithelium. Renewal is controlled by interplay between signalling pathways, among which canonical and non-canonical Wnt signals play prominent roles. Overall 92% of colon tumours show increased canonical Wnt signalling resulting from mutations, established as major driver steps towards carcinogenesis.
    Results: Here, we examined the physiological role of RhoU/Wrch1 in gut homeostasis. RhoU is an atypical Rho GTPase related to Cdc42/Rac1 and identified as a transcriptional target of non-canonical Wnt signalling. We found that RHOU expression is reduced in human colorectal tumour samples. We show that RhoU is mainly expressed in the differentiated compartment of the gut epithelium. Rhou specific invalidation in the mouse gut elicits cell hyperplasia and is associated in the colon with a highly disorganized luminal epithelium. Hyperplasia affects all cell types in the small intestine and colon and has a higher impact on goblet cells. Hyperplasia is associated with a reduction of apoptosis and an increased proliferation. RhoU knockdown in human DLD-1 colon cancer cells also elicits a higher growth index and reduces cell apoptosis. Last, loss of RhoU function in the mouse gut epithelium or in DLD-1 cells increases RhoA activity and the level of phosphorylated Myosin Light Chain-2, which may functionally link RhoU activity to apoptosis.
    Conclusion: RhoU is mostly expressed in the differentiated compartment of the gut. It plays a role in homeostasis as its specific invalidation elicits hyperplasia of all cell types. This mainly results from a reduction of apoptosis, through actomyosin-dependent mechanisms.
    Significance: RhoU negatively controls cell growth in the intestinal epithelium. Since its expression is sensitive to non-canonical Wnt signals and is reduced in colorectal tumours, downregulating RhoU may thus have an instrumental role in tumour progression.
    MeSH term(s) Animals ; Apoptosis ; Cell Differentiation ; Cell Line, Tumor ; Cell Proliferation ; Colorectal Neoplasms/enzymology ; Colorectal Neoplasms/pathology ; Goblet Cells/enzymology ; Goblet Cells/pathology ; Humans ; Hyperplasia ; Intestinal Mucosa/enzymology ; Intestinal Mucosa/pathology ; Mice, Inbred C57BL ; Wnt Signaling Pathway ; rho GTP-Binding Proteins/genetics ; rho GTP-Binding Proteins/metabolism
    Chemical Substances RHOU protein, human (EC 3.6.1.-) ; RhoU protein, mouse (EC 3.6.5.2) ; rho GTP-Binding Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2019-03-12
    Publishing country England
    Document type Journal Article
    ZDB-ID 245745-3
    ISSN 1768-322X ; 0399-0311 ; 0248-4900
    ISSN (online) 1768-322X
    ISSN 0399-0311 ; 0248-4900
    DOI 10.1111/boc.201800062
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. Article ; Online: SOX9 has distinct regulatory roles in alternative splicing and transcription.

    Girardot, Michael / Bayet, Elsa / Maurin, Justine / Fort, Philippe / Roux, Pierre / Raynaud, Peggy

    Nucleic acids research

    2018  Volume 46, Issue 17, Page(s) 9106–9118

    Abstract: SOX9 is known as a crucial transcription factor for various developmental processes and for tissue homeostasis. We examined here its potential role in alternative splicing by analyzing global splicing changes, using RNA-seq of colon tumor cells. We show ... ...

    Abstract SOX9 is known as a crucial transcription factor for various developmental processes and for tissue homeostasis. We examined here its potential role in alternative splicing by analyzing global splicing changes, using RNA-seq of colon tumor cells. We show that SOX9 knockdown alters the splicing of hundreds of genes without affecting their expression levels, revealing that SOX9 controls distinct splicing and transcriptional programs. SOX9 does not affect splicing patterns through the control of splicing factors expression. We identify mutants that uncouple SOX9 splicing function from its transcriptional activity. We demonstrate that SOX9 binds to RNA and associates with several RNA-binding proteins, including the core exon junction complex component Y14. Half of SOX9 splicing targets are also modulated by Y14 and are no longer regulated by SOX9 upon Y14 depletion. Altogether, our work reveals that SOX9 is a moonlighting protein which modulates either transcription or splicing of distinct sets of targets.
    MeSH term(s) Alternative Splicing/genetics ; Cells, Cultured ; Gene Expression Regulation ; Gene Knockdown Techniques ; HEK293 Cells ; Humans ; Protein Binding ; RNA Splicing/genetics ; RNA, Messenger/metabolism ; RNA-Binding Proteins/metabolism ; SOX9 Transcription Factor/physiology ; Transcription, Genetic/genetics
    Chemical Substances RBM8A protein, human ; RNA, Messenger ; RNA-Binding Proteins ; SOX9 Transcription Factor ; SOX9 protein, human
    Language English
    Publishing date 2018-09-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    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/gky553
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  4. Article ; Online: Ensa controls S-phase length by modulating Treslin levels.

    Charrasse, Sophie / Gharbi-Ayachi, Aicha / Burgess, Andrew / Vera, Jorge / Hached, Khaled / Raynaud, Peggy / Schwob, Etienne / Lorca, Thierry / Castro, Anna

    Nature communications

    2017  Volume 8, Issue 1, Page(s) 206

    Abstract: The Greatwall/Ensa/PP2A-B55 pathway is essential for controlling mitotic substrate phosphorylation and mitotic entry. Here, we investigate the effect of the knockdown of the Gwl substrate, Ensa, in human cells. Unexpectedly, Ensa knockdown promotes a ... ...

    Abstract The Greatwall/Ensa/PP2A-B55 pathway is essential for controlling mitotic substrate phosphorylation and mitotic entry. Here, we investigate the effect of the knockdown of the Gwl substrate, Ensa, in human cells. Unexpectedly, Ensa knockdown promotes a dramatic extension of S phase associated with a lowered density of replication forks. Notably, Ensa depletion results in a decrease of Treslin levels, a pivotal protein for the firing of replication origins. Accordingly, the extended S phase in Ensa-depleted cells is completely rescued by the overexpression of Treslin. Our data herein reveal a new mechanism by which normal cells regulate S-phase duration by controlling the ubiquitin-proteasome degradation of Treslin in a Gwl/Ensa-dependent pathway.The Greatwall/Ensa/PP2A-B55 pathway controls mitotic substrate phosphorylation and mitotic entry. Here the authors show that cells regulate S phase duration by controlling the ubiquitin-proteasome degradation of Treslin in a Gwl/Ensa-dependent pathway.
    MeSH term(s) Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Division ; HeLa Cells ; Humans ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Mitosis ; Peptides/genetics ; Peptides/metabolism ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; S Phase
    Chemical Substances Cell Cycle Proteins ; Microtubule-Associated Proteins ; Peptides ; TICRR protein, human ; endosulfine ; MASTL protein, human (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2017--08
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2041-1723
    ISSN (online) 2041-1723
    DOI 10.1038/s41467-017-00339-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  5. Article ; Online: IL-24 contributes to skin inflammation in Para-Phenylenediamine-induced contact hypersensitivity.

    Van Belle, Astrid B / Cochez, Perrine M / de Heusch, Magali / Pointner, Lisa / Opsomer, Remi / Raynaud, Peggy / Achouri, Younes / Hendrickx, Emilie / Cheou, Pamela / Warnier, Guy / Renauld, Jean-Christophe / Baeck, Marie / Dumoutier, Laure

    Scientific reports

    2019  Volume 9, Issue 1, Page(s) 1852

    Abstract: Para-Phenylenediamine (PPD) is an aromatic amine used in hair dyes and in temporary black henna tattoos, which is a frequent cause of allergic contact dermatitis (ACD). ACD is a skin inflammatory reaction characterized by modifications such as spongiosis, ...

    Abstract Para-Phenylenediamine (PPD) is an aromatic amine used in hair dyes and in temporary black henna tattoos, which is a frequent cause of allergic contact dermatitis (ACD). ACD is a skin inflammatory reaction characterized by modifications such as spongiosis, exocytosis and acanthosis. The aim of this study is to characterize the expression and the role of IL-20-related cytokines, including IL-19, IL-20, IL-22 and IL-24, in ACD. The expression of IL19, IL20, IL22 and IL24 is increased in affected skin from PPD allergic patients compared with uninvolved skin. In addition, the expression of these cytokines positively correlates with clinical symptoms. To assess their role in ACD, we set up a mouse model of PPD-induced allergic contact dermatitis and we showed that, in contrast to Il22-deficient mice, Il22ra1-, Il20rb- and Il24-deficient mice are partially protected against development of PPD-induced contact hypersensitivity. These mice have decreased ear thickening and less acanthosis compared with WT mice after PPD treatment. In addition, the absence of IL-22R, IL-20R2 or IL-24 affects the recruitment of neutrophils into the skin but not the total IgE production. Taken together, these results demonstrate the implication of IL-24 via the IL-20R type II receptor in the inflammatory process of ACD.
    MeSH term(s) Adult ; Aged ; Animals ; Biopsy ; Coloring Agents ; Cytokines/metabolism ; Dermatitis, Allergic Contact/metabolism ; Disease Models, Animal ; Humans ; Immunoglobulin E/metabolism ; Inflammation/chemically induced ; Inflammation/metabolism ; Interleukins/metabolism ; Leukocyte Common Antigens/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Middle Aged ; Phenylenediamines ; Receptors, Interleukin/metabolism ; Skin/drug effects ; Skin/metabolism ; Interleukin-22
    Chemical Substances Coloring Agents ; Cytokines ; Il24 protein, mouse ; Interleukins ; Phenylenediamines ; Receptors, Interleukin ; interleukin-20 receptor ; interleukin-22 receptor ; interleukin-24 ; Immunoglobulin E (37341-29-0) ; Leukocyte Common Antigens (EC 3.1.3.48) ; 4-phenylenediamine (U770QIT64J) ; interleukin 20 (U91R7IMG8U)
    Language English
    Publishing date 2019-02-12
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-018-38156-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  6. Article ; Online: Biliary differentiation and bile duct morphogenesis in development and disease.

    Raynaud, Peggy / Carpentier, Rodolphe / Antoniou, Aline / Lemaigre, Frédéric P

    The international journal of biochemistry & cell biology

    2011  Volume 43, Issue 2, Page(s) 245–256

    Abstract: The biliary tract consists of a network of intrahepatic and extrahepatic ducts that collect and drain the bile produced by hepatocytes to the gut. The bile ducts are lined by cholangiocytes, a specialized epithelial cell type that has a dual origin. ... ...

    Abstract The biliary tract consists of a network of intrahepatic and extrahepatic ducts that collect and drain the bile produced by hepatocytes to the gut. The bile ducts are lined by cholangiocytes, a specialized epithelial cell type that has a dual origin. Intrahepatic cholangiocytes derive from the liver precursor cells, whereas extrahepatic cholangiocytes are generated directly from the endoderm. In this review we discuss the mechanisms of cholangiocyte differentiation and bile duct morphogenesis, and describe how developing ducts interact with the hepatic artery. We also present an overview of the mechanisms of biliary dysgenesis in humans.
    MeSH term(s) Animals ; Bile Ducts/embryology ; Bile Ducts/growth & development ; Bile Ducts/pathology ; Biliary Tract/embryology ; Biliary Tract/growth & development ; Biliary Tract Diseases/genetics ; Biliary Tract Diseases/pathology ; Cell Differentiation ; Gene Expression Regulation, Developmental ; Hepatocytes/cytology ; Humans ; Liver/embryology ; Liver/growth & development ; Liver/pathology ; Liver Diseases/genetics ; Liver Diseases/pathology ; MicroRNAs/physiology ; Morphogenesis ; Signal Transduction
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2011-02
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1228429-4
    ISSN 1878-5875 ; 1357-2725
    ISSN (online) 1878-5875
    ISSN 1357-2725
    DOI 10.1016/j.biocel.2009.07.020
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  7. Article ; Online: MiR-495 and miR-218 regulate the expression of the Onecut transcription factors HNF-6 and OC-2.

    Simion, Alexandru / Laudadio, Ilaria / Prévot, Pierre-Paul / Raynaud, Peggy / Lemaigre, Frédéric P / Jacquemin, Patrick

    Biochemical and biophysical research communications

    2010  Volume 391, Issue 1, Page(s) 293–298

    Abstract: MicroRNAs are small, non-coding RNAs that posttranscriptionally regulate gene expression mainly by binding to the 3'UTR of their target mRNAs. Recent data revealed that microRNAs have an important role in pancreas and liver development and physiology. ... ...

    Abstract MicroRNAs are small, non-coding RNAs that posttranscriptionally regulate gene expression mainly by binding to the 3'UTR of their target mRNAs. Recent data revealed that microRNAs have an important role in pancreas and liver development and physiology. Using cloning and microarray profiling approaches, we show that a unique repertoire of microRNAs is expressed at the onset of liver and pancreas organogenesis, and in pancreas and liver at key stages of cell fate determination. Among the microRNAs that are expressed at these stages, miR-495 and miR-218 were predicted to, respectively, target the Onecut (OC) transcription factors Hepatocyte Nuclear Factor-6 (HNF-6/OC-1) and OC-2, two important regulators of liver and pancreas development. MiR-495 and miR-218 are dynamically expressed in developing liver and pancreas, and by transient transfection, we show that they target HNF-6 and OC-2 3'UTRs. Moreover, when overexpressed in cultured cells, miR-495 and miR-218 decrease the endogenous levels of HNF-6 and OC-2 mRNA. These results indicate that the expression of regulators of liver and pancreas development is modulated by microRNAs. They also suggest a developmental role for miR-495 and miR-218.
    MeSH term(s) Animals ; Base Sequence ; Cell Line ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Hepatocyte Nuclear Factor 6/genetics ; Homeodomain Proteins/biosynthesis ; Homeodomain Proteins/genetics ; Humans ; Liver/embryology ; Liver/metabolism ; Mice ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Molecular Sequence Data ; Onecut Transcription Factors/biosynthesis ; Onecut Transcription Factors/genetics ; Pancreas/embryology ; Pancreas/metabolism ; Protein Biosynthesis/genetics ; Transcription Factors/biosynthesis ; Transcription Factors/genetics
    Chemical Substances Hepatocyte Nuclear Factor 6 ; Homeodomain Proteins ; MIRN218 microRNA, mouse ; MIRN495 microRNA, mouse ; MicroRNAs ; ONECUT2 protein, mouse ; Onecut Transcription Factors ; Onecut1 protein, mouse ; Transcription Factors
    Language English
    Publishing date 2010-01-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2009.11.052
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  8. Article: Notch signaling controls liver development by regulating biliary differentiation.

    Zong, Yiwei / Panikkar, Archana / Xu, Jie / Antoniou, Aline / Raynaud, Peggy / Lemaigre, Frederic / Stanger, Ben Z

    Development (Cambridge, England)

    2009  Volume 136, Issue 10, Page(s) 1727–1739

    Abstract: In the mammalian liver, bile is transported to the intestine through an intricate network of bile ducts. Notch signaling is required for normal duct formation, but its mode of action has been unclear. Here, we show in mice that bile ducts arise through a ...

    Abstract In the mammalian liver, bile is transported to the intestine through an intricate network of bile ducts. Notch signaling is required for normal duct formation, but its mode of action has been unclear. Here, we show in mice that bile ducts arise through a novel mechanism of tubulogenesis involving sequential radial differentiation. Notch signaling is activated in a subset of liver progenitor cells fated to become ductal cells, and pathway activation is necessary for biliary fate. Notch signals are also required for bile duct morphogenesis, and activation of Notch signaling in the hepatic lobule promotes ectopic biliary differentiation and tubule formation in a dose-dependent manner. Remarkably, activation of Notch signaling in postnatal hepatocytes causes them to adopt a biliary fate through a process of reprogramming that recapitulates normal bile duct development. These results reconcile previous conflicting reports about the role of Notch during liver development and suggest that Notch acts by coordinating biliary differentiation and morphogenesis.
    MeSH term(s) Animals ; Animals, Newborn ; Antigens, Differentiation/metabolism ; Bile Ducts/cytology ; Bile Ducts/embryology ; Bile Ducts/growth & development ; Cell Differentiation/physiology ; Hepatocytes/cytology ; Liver/cytology ; Liver/embryology ; Liver/growth & development ; Mice ; Mice, Mutant Strains ; Morphogenesis ; Receptors, Notch/physiology ; Signal Transduction/physiology
    Chemical Substances Antigens, Differentiation ; Receptors, Notch
    Language English
    Publishing date 2009-04-15
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.029140
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  9. Article: Correlation between bovine calpastatin mRNA transcripts and protein isoforms.

    Raynaud, Peggy / Gillard, Mélanie / Parr, Tim / Bardsley, Ronald / Amarger, Valérie / Levéziel, Hubert

    Archives of biochemistry and biophysics

    2005  Volume 440, Issue 1, Page(s) 46–53

    Abstract: Calpastatin is a specific calpain protease inhibitor: calpains are a family of calcium-activated neutral proteases, which have been implicated in various processes. Despite all the available data concerning calpastatin, little is known about how this ... ...

    Abstract Calpastatin is a specific calpain protease inhibitor: calpains are a family of calcium-activated neutral proteases, which have been implicated in various processes. Despite all the available data concerning calpastatin, little is known about how this gene is regulated, particularly in bovine. The existence of four types of transcripts differing at their 5' ends (Type I, II, III, and IV) has been demonstrated. Here, we show that the Type I, II, and III transcripts are ubiquitous while Type IV is testis-specific. In addition, a Northern blot analysis revealed that the Type III transcript may have three different 3' termini. Using specific anti-peptide anti-sera, a correspondence between a 145 and a 125 kDa isoforms, and Type I and/or II and III transcripts, respectively, has been established. Finally, we discuss the origin of a 70 kDa isoform, recognized by anti-sera directed against the N-terminal region.
    MeSH term(s) Animals ; Base Sequence ; Blotting, Northern ; Calcium-Binding Proteins/genetics ; Calcium-Binding Proteins/metabolism ; Cattle ; Cysteine Proteinase Inhibitors/pharmacology ; Immune Sera ; Male ; Molecular Sequence Data ; Molecular Weight ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Transcription, Genetic
    Chemical Substances Calcium-Binding Proteins ; Cysteine Proteinase Inhibitors ; Immune Sera ; Protein Isoforms ; RNA, Messenger ; calpastatin (79079-11-1)
    Language English
    Publishing date 2005-07-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 523-x
    ISSN 1096-0384 ; 0003-9861
    ISSN (online) 1096-0384
    ISSN 0003-9861
    DOI 10.1016/j.abb.2005.05.028
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  10. Article: Four promoters direct expression of the calpastatin gene.

    Raynaud, Peggy / Jayat-Vignoles, Chantal / Laforêt, Marie-Pierre / Levéziel, Hubert / Amarger, Valérie

    Archives of biochemistry and biophysics

    2005  Volume 437, Issue 1, Page(s) 69–77

    Abstract: Calpastatin is a specific endogenous protein inhibitor of the ubiquitous calcium dependent proteinases mu- and m-calpain. The calpain-calpastatin system is involved in various physiological and pathological processes. In the present study, we determined ... ...

    Abstract Calpastatin is a specific endogenous protein inhibitor of the ubiquitous calcium dependent proteinases mu- and m-calpain. The calpain-calpastatin system is involved in various physiological and pathological processes. In the present study, we determined the bovine calpastatin gene structure and demonstrated that four promoters direct its expression. The gene harbours 35 exons spanning at least 130kb on genomic DNA. Its structure is similar to that of mouse, pig, and human gene. Transient transfection assays in both C2C12 and COS7 cell lines demonstrated that the putative promoter regions situated 5' to exon 1xa, 1xb, 1u, and 14t were functional. We also established that the region situated upstream exon 14t is subjected to a tissue specific regulation. The implication of numerous high-scoring cis acting transcriptional motifs which are present in these regions will need to be determined. The existence of four promoters suggests differential expression patterns which must have a physiological significance.
    MeSH term(s) 5' Flanking Region/genetics ; Animals ; Base Sequence ; COS Cells ; Calcium-Binding Proteins/genetics ; Cattle ; Cercopithecus aethiops ; Exons/genetics ; Gene Expression Regulation/genetics ; Molecular Sequence Data ; Organ Specificity/genetics ; Promoter Regions, Genetic
    Chemical Substances Calcium-Binding Proteins ; calpastatin (79079-11-1)
    Language English
    Publishing date 2005-05-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 523-x
    ISSN 1096-0384 ; 0003-9861
    ISSN (online) 1096-0384
    ISSN 0003-9861
    DOI 10.1016/j.abb.2005.02.026
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top