The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform

Deborah L Gumucio - One of the best experts on this subject based on the ideXlab platform.

  • cis elements of the villin gene Control Expression in restricted domains of the vertical crypt and horizontal duodenum cecum axes of the intestine
    Journal of Biological Chemistry, 2002
    Co-Authors: Blair B Madison, Laura Dunbar, Xiaotan T Qiao, Katherine Braunstein, Evan M Braunstein, Deborah L Gumucio
    Abstract:

    Abstract Villin, an actin bundling protein found in the apical brush border of absorptive tissues, is one of the first structural genes to be transcriptionally activated in the embryonic intestinal endoderm. In the adult, villin is broadly expressed in every cell of the intestinal epithelium on both the vertical axis (crypt to villus tip) and the horizontal axis (duodenum through colon) of the intestine. Here, we document that a 12.4-kilobase region of the mouse villin gene drives high level Expression of two different reporter genes (LacZ and Cre recombinase) within the entire intestinal epithelium of transgenic mice. Deletion of a portion of this transgene results in reduction of β-galactosidase activity in restricted domains of the small intestine (duodenum) and large intestine (cecum). In addition, Expression is reduced in the crypt compartment throughout the intestine. Thus, the global Expression pattern of villin in the intestine is apparently the consequence of an amalgam of distinct and individual domain-specific Control processes. That is, Expression of villin in the duodenum and cecum requires different regulatory sequences than the rest of the intestine, and the Expression of villin in crypts is regulated by different circuitry than Expression of villin on villus tips.

  • cis elements of the villin gene Control Expression in restricted domains of the vertical crypt and horizontal duodenum cecum axes of the intestine
    Journal of Biological Chemistry, 2002
    Co-Authors: Blair B Madison, Laura Dunbar, Xiaotan T Qiao, Katherine Braunstein, Evan M Braunstein, Deborah L Gumucio
    Abstract:

    Villin, an actin bundling protein found in the apical brush border of absorptive tissues, is one of the first structural genes to be transcriptionally activated in the embryonic intestinal endoderm. In the adult, villin is broadly expressed in every cell of the intestinal epithelium on both the vertical axis (crypt to villus tip) and the horizontal axis (duodenum through colon) of the intestine. Here, we document that a 12.4-kilobase region of the mouse villin gene drives high level Expression of two different reporter genes (LacZ and Cre recombinase) within the entire intestinal epithelium of transgenic mice. Deletion of a portion of this transgene results in reduction of beta-galactosidase activity in restricted domains of the small intestine (duodenum) and large intestine (cecum). In addition, Expression is reduced in the crypt compartment throughout the intestine. Thus, the global Expression pattern of villin in the intestine is apparently the consequence of an amalgam of distinct and individual domain-specific Control processes. That is, Expression of villin in the duodenum and cecum requires different regulatory sequences than the rest of the intestine, and the Expression of villin in crypts is regulated by different circuitry than Expression of villin on villus tips.

Gerard Karsenty - One of the best experts on this subject based on the ideXlab platform.

  • two distinct osteoblast specific cis acting elements Control Expression of a mouse osteocalcin gene
    Molecular and Cellular Biology, 1995
    Co-Authors: Patricia Ducy, Gerard Karsenty
    Abstract:

    Osteoblasts are cells of mesodermal origin that play a pivotal role during bone growth and mineralization. The mechanisms governing osteoblast-specific gene Expression are still unknown. To understand these mechanisms, we analyzed the cis-acting elements of mouse osteocalcin gene 2 (mOG2), the best-characterized osteoblast-specific gene, by DNA transfection experiments in osteoblastic and nonosteoblastic cell lines and by DNA-binding assays. 5' deletion analysis of an mOG2 promoter-luciferase chimeric gene showed that a region located between -147 and -34 contained most if not all of the regulatory elements required for osteoblast-specific Expression. Three different binding sites, called A, B, and C, for factors present in nuclear extracts of osteoblasts were identified in this short promoter by DNase I footprint assays. In gel retardation assays, the A element, located between bp -64 and -47, bound a factor present only in nuclear extracts of osteoblastic cell lines and nonmineralizing primary osteoblasts. The B element, located between bp -110 and -83, bound a ubiquitously expressed factor. The C element, located between bp -146 and -132, bound a factor present only in nuclear extracts of osteoblastic cell lines and nonmineralizing and mineralizing primary osteoblasts. When cloned upstream of a minimum osteocalcin promoter or a heterologous promoter, multimers of the A element strongly increased the activities of these promoters in osteoblastic cell lines at two different stages of differentiation but in no other cell line; we named this element osteocalcin-specific element 1 (OSE1). Multimers of the C element increased the activities of these promoters predominantly in a differentiated osteoblastic cell line; we named this element OSE2. This study demonstrates that two distinct cis-acting elements are responsible for osteoblast Expression of mOG2 and provides for the first time a functional characterization of osteoblast-specific cis-acting elements. We speculate that these two elements may be important at several stages of osteoblast differentiation.

  • two distinct osteoblast specific cis acting elements Control Expression of a mouse osteocalcin gene
    Molecular and Cellular Biology, 1995
    Co-Authors: Patricia Ducy, Gerard Karsenty
    Abstract:

    Osteoblasts are cells of mesodermal origin that play a pivotal role during bone growth and mineralization. The mechanisms governing osteoblast-specific gene Expression are still unknown. To understand these mechanisms, we analyzed the cis-acting elements of mouse osteocalcin gene 2 (mOG2), the best-characterized osteoblast-specific gene, by DNA transfection experiments in osteoblastic and nonosteoblastic cell lines and by DNA-binding assays. 5' deletion analysis of an mOG2 promoter-luciferase chimeric gene showed that a region located between -147 and -34 contained most if not all of the regulatory elements required for osteoblast-specific Expression. Three different binding sites, called A, B, and C, for factors present in nuclear extracts of osteoblasts were identified in this short promoter by DNase I footprint assays. In gel retardation assays, the A element, located between bp -64 and -47, bound a factor present only in nuclear extracts of osteoblastic cell lines and nonmineralizing primary osteoblasts. The B element, located between bp -110 and -83, bound a ubiquitously expressed factor. The C element, located between bp -146 and -132, bound a factor present only in nuclear extracts of osteoblastic cell lines and nonmineralizing and mineralizing primary osteoblasts. When cloned upstream of a minimum osteocalcin promoter or a heterologous promoter, multimers of the A element strongly increased the activities of these promoters in osteoblastic cell lines at two different stages of differentiation but in no other cell line; we named this element osteocalcin-specific element 1 (OSE1). Multimers of the C element increased the activities of these promoters predominantly in a differentiated osteoblastic cell line; we named this element OSE2. This study demonstrates that two distinct cis-acting elements are responsible for osteoblast Expression of mOG2 and provides for the first time a functional characterization of osteoblast-specific cis-acting elements. We speculate that these two elements may be important at several stages of osteoblast differentiation.

Blair B Madison - One of the best experts on this subject based on the ideXlab platform.

  • cis elements of the villin gene Control Expression in restricted domains of the vertical crypt and horizontal duodenum cecum axes of the intestine
    Journal of Biological Chemistry, 2002
    Co-Authors: Blair B Madison, Laura Dunbar, Xiaotan T Qiao, Katherine Braunstein, Evan M Braunstein, Deborah L Gumucio
    Abstract:

    Abstract Villin, an actin bundling protein found in the apical brush border of absorptive tissues, is one of the first structural genes to be transcriptionally activated in the embryonic intestinal endoderm. In the adult, villin is broadly expressed in every cell of the intestinal epithelium on both the vertical axis (crypt to villus tip) and the horizontal axis (duodenum through colon) of the intestine. Here, we document that a 12.4-kilobase region of the mouse villin gene drives high level Expression of two different reporter genes (LacZ and Cre recombinase) within the entire intestinal epithelium of transgenic mice. Deletion of a portion of this transgene results in reduction of β-galactosidase activity in restricted domains of the small intestine (duodenum) and large intestine (cecum). In addition, Expression is reduced in the crypt compartment throughout the intestine. Thus, the global Expression pattern of villin in the intestine is apparently the consequence of an amalgam of distinct and individual domain-specific Control processes. That is, Expression of villin in the duodenum and cecum requires different regulatory sequences than the rest of the intestine, and the Expression of villin in crypts is regulated by different circuitry than Expression of villin on villus tips.

  • cis elements of the villin gene Control Expression in restricted domains of the vertical crypt and horizontal duodenum cecum axes of the intestine
    Journal of Biological Chemistry, 2002
    Co-Authors: Blair B Madison, Laura Dunbar, Xiaotan T Qiao, Katherine Braunstein, Evan M Braunstein, Deborah L Gumucio
    Abstract:

    Villin, an actin bundling protein found in the apical brush border of absorptive tissues, is one of the first structural genes to be transcriptionally activated in the embryonic intestinal endoderm. In the adult, villin is broadly expressed in every cell of the intestinal epithelium on both the vertical axis (crypt to villus tip) and the horizontal axis (duodenum through colon) of the intestine. Here, we document that a 12.4-kilobase region of the mouse villin gene drives high level Expression of two different reporter genes (LacZ and Cre recombinase) within the entire intestinal epithelium of transgenic mice. Deletion of a portion of this transgene results in reduction of beta-galactosidase activity in restricted domains of the small intestine (duodenum) and large intestine (cecum). In addition, Expression is reduced in the crypt compartment throughout the intestine. Thus, the global Expression pattern of villin in the intestine is apparently the consequence of an amalgam of distinct and individual domain-specific Control processes. That is, Expression of villin in the duodenum and cecum requires different regulatory sequences than the rest of the intestine, and the Expression of villin in crypts is regulated by different circuitry than Expression of villin on villus tips.

Patricia Ducy - One of the best experts on this subject based on the ideXlab platform.

  • two distinct osteoblast specific cis acting elements Control Expression of a mouse osteocalcin gene
    Molecular and Cellular Biology, 1995
    Co-Authors: Patricia Ducy, Gerard Karsenty
    Abstract:

    Osteoblasts are cells of mesodermal origin that play a pivotal role during bone growth and mineralization. The mechanisms governing osteoblast-specific gene Expression are still unknown. To understand these mechanisms, we analyzed the cis-acting elements of mouse osteocalcin gene 2 (mOG2), the best-characterized osteoblast-specific gene, by DNA transfection experiments in osteoblastic and nonosteoblastic cell lines and by DNA-binding assays. 5' deletion analysis of an mOG2 promoter-luciferase chimeric gene showed that a region located between -147 and -34 contained most if not all of the regulatory elements required for osteoblast-specific Expression. Three different binding sites, called A, B, and C, for factors present in nuclear extracts of osteoblasts were identified in this short promoter by DNase I footprint assays. In gel retardation assays, the A element, located between bp -64 and -47, bound a factor present only in nuclear extracts of osteoblastic cell lines and nonmineralizing primary osteoblasts. The B element, located between bp -110 and -83, bound a ubiquitously expressed factor. The C element, located between bp -146 and -132, bound a factor present only in nuclear extracts of osteoblastic cell lines and nonmineralizing and mineralizing primary osteoblasts. When cloned upstream of a minimum osteocalcin promoter or a heterologous promoter, multimers of the A element strongly increased the activities of these promoters in osteoblastic cell lines at two different stages of differentiation but in no other cell line; we named this element osteocalcin-specific element 1 (OSE1). Multimers of the C element increased the activities of these promoters predominantly in a differentiated osteoblastic cell line; we named this element OSE2. This study demonstrates that two distinct cis-acting elements are responsible for osteoblast Expression of mOG2 and provides for the first time a functional characterization of osteoblast-specific cis-acting elements. We speculate that these two elements may be important at several stages of osteoblast differentiation.

  • two distinct osteoblast specific cis acting elements Control Expression of a mouse osteocalcin gene
    Molecular and Cellular Biology, 1995
    Co-Authors: Patricia Ducy, Gerard Karsenty
    Abstract:

    Osteoblasts are cells of mesodermal origin that play a pivotal role during bone growth and mineralization. The mechanisms governing osteoblast-specific gene Expression are still unknown. To understand these mechanisms, we analyzed the cis-acting elements of mouse osteocalcin gene 2 (mOG2), the best-characterized osteoblast-specific gene, by DNA transfection experiments in osteoblastic and nonosteoblastic cell lines and by DNA-binding assays. 5' deletion analysis of an mOG2 promoter-luciferase chimeric gene showed that a region located between -147 and -34 contained most if not all of the regulatory elements required for osteoblast-specific Expression. Three different binding sites, called A, B, and C, for factors present in nuclear extracts of osteoblasts were identified in this short promoter by DNase I footprint assays. In gel retardation assays, the A element, located between bp -64 and -47, bound a factor present only in nuclear extracts of osteoblastic cell lines and nonmineralizing primary osteoblasts. The B element, located between bp -110 and -83, bound a ubiquitously expressed factor. The C element, located between bp -146 and -132, bound a factor present only in nuclear extracts of osteoblastic cell lines and nonmineralizing and mineralizing primary osteoblasts. When cloned upstream of a minimum osteocalcin promoter or a heterologous promoter, multimers of the A element strongly increased the activities of these promoters in osteoblastic cell lines at two different stages of differentiation but in no other cell line; we named this element osteocalcin-specific element 1 (OSE1). Multimers of the C element increased the activities of these promoters predominantly in a differentiated osteoblastic cell line; we named this element OSE2. This study demonstrates that two distinct cis-acting elements are responsible for osteoblast Expression of mOG2 and provides for the first time a functional characterization of osteoblast-specific cis-acting elements. We speculate that these two elements may be important at several stages of osteoblast differentiation.

Lydia Michaut - One of the best experts on this subject based on the ideXlab platform.

  • Pillars article: the dorsoventral regulatory gene cassette spätzle/Toll/cactus Controls the potent antifungal response in Drosophila adults. Cell. 1996. 86: 973-983
    Journal of Immunology, 2012
    Co-Authors: Bruno Lemaitre, Lydia Michaut, Emmanuelle Nicolas, Jules Hoffmann
    Abstract:

    The cytokine-induced activation cascade of NF-kappaB in mammals and the activation of the morphogen dorsal in Drosophila embryos show striking structural and functional similarities (Toll/IL-1, Cactus/I-kappaB, and dorsal/NF-kappaB). Here we demonstrate that these parallels extend to the immune response of Drosophila. In particular, the intracellular components of the dorsoventral signaling pathway (except for dorsal) and the extracellular Toll ligand, spätzle regulatory gene cassette, Control Expression of the antifungal peptide gene drosomycin in adults. We also show that mutations in the Toll signaling pathway dramatically reduce survival after fungal infection. Antibacterial genes are induced either by a distinct pathway involving the immune deficiency gene (imd) or by combined activation of both imd and dorsoventral pathways.

  • the dorsoventral regulatory gene cassette spatzle toll cactus Controls the potent antifungal response in drosophila adults
    Cell, 1996
    Co-Authors: Bruno Lemaitre, Emmanuelle Nicolas, Lydia Michaut
    Abstract:

    The cytokine-induced activation cascade of NF-kappaB in mammals and the activation of the morphogen dorsal in Drosophila embryos show striking structural and functional similarities (Toll/IL-1, Cactus/I-kappaB, and dorsal/NF-kappaB). Here we demonstrate that these parallels extend to the immune response of Drosophila. In particular, the intracellular components of the dorsoventral signaling pathway (except for dorsal) and the extracellular Toll ligand, spatzle, Control Expression of the antifungal peptide gene drosomycin in adults. We also show that mutations in the Toll signaling pathway dramatically reduce survival after fungal infection. Antibacterial genes are induced either by a distinct pathway involving the immune deficiency gene (imd) or by combined activation of both imd and dorsoventral pathways.