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  • 1
    Online Resource
    Online Resource
    High-Throughput Gene Discovery in the Rat
    Cold Spring Harbor Laboratory ; 2004
    In:  Genome Research Vol. 14, No. 4 ( 2004-04), p. 733-741
    Details
    In: Genome Research, Cold Spring Harbor Laboratory, Vol. 14, No. 4 ( 2004-04), p. 733-741
    Abstract: The rat is an important animal model for human diseases and is widely used in physiology. In this article we present a new strategy for gene discovery based on the production of ESTs from serially subtracted and normalized cDNA libraries, and we describe its application for the development of a comprehensive nonredundant collection of rat ESTs. Our new strategy appears to yield substantially more EST clusters per ESTs sequenced than do previous approaches that did not use serial subtraction. However, multiple rounds of library subtraction resulted in high frequencies of otherwise rare internally primed cDNAs, defining the limits of this powerful approach. To date, we have generated 〉 200,000 3′ ESTs from 〉 100 cDNA libraries representing a wide range of tissues and developmental stages of the laboratory rat. Most importantly, we have contributed to ∼50,000 rat UniGene clusters. We have identified, arrayed, and derived 5′ ESTs from 〉 30,000 unique rat cDNA clones. Complete information, including radiation hybrid mapping data, is also maintained locally at http://genome.uiowa.edu/clcg.html. All of the sequences described in this article have been submitted to the dbEST division of the NCBI.
    Type of Medium: Online Resource
    ISSN: 1088-9051
    URL: Article
    DOI: 10.1101/gr.1414204
    RVK:
    XA 10000
    Language: English
    Publisher: Cold Spring Harbor Laboratory
    Publication Date: 2004
    detail.hit.zdb_id: 1483456-X
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Loss of mXinα, an intercalated disk protein, results in cardiac hypertrophy and cardiomyopathy with conduction defects
    American Physiological Society ; 2007
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 293, No. 5 ( 2007-11), p. H2680-H2692
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 293, No. 5 ( 2007-11), p. H2680-H2692
    Abstract: The intercalated disk protein Xin was originally discovered in chicken striated muscle and implicated in cardiac morphogenesis. In the mouse, there are two homologous genes, mXinα and mXinβ. The human homolog of mXinα, Cmya1, maps to chromosomal region 3p21.2–21.3, near a dilated cardiomyopathy with conduction defect-2 locus. Here we report that mXinα-null mouse hearts are hypertrophied and exhibit fibrosis, indicative of cardiomyopathy. A significant upregulation of mXinβ likely provides partial compensation and accounts for the viability of the mXinα-null mice. Ultrastructural studies of mXinα-null mouse hearts reveal intercalated disk disruption and myofilament disarray. In mXinα-null mice, there is a significant decrease in the expression level of p120-catenin, β-catenin, N-cadherin, and desmoplakin, which could compromise the integrity of the intercalated disks and functionally weaken adhesion, leading to cardiac defects. Additionally, altered localization and decreased expression of connexin 43 are observed in the mXinα-null mouse heart, which, together with previously observed abnormal electrophysiological properties of mXinα-deficient mouse ventricular myocytes, could potentially lead to conduction defects. Indeed, ECG recordings on isolated, perfused hearts (Langendorff preparations) show a significantly prolonged QT interval in mXinα-deficient hearts. Thus mXinα functions in regulating the hypertrophic response and maintaining the structural integrity of the intercalated disk in normal mice, likely through its association with adherens junctional components and actin cytoskeleton. The mXinα-knockout mouse line provides a novel model of cardiac hypertrophy and cardiomyopathy with conduction defects.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00806.2007
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2007
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Nuclear proteins of the bovine esophageal epithelium: I. Monoclonal antibody W2 specifically reacts with condensed nuclei of differentiated superficial cells
    The Company of Biologists ; 1993
    In:  Journal of Cell Science Vol. 104, No. 2 ( 1993-02-01), p. 237-247
    Details
    In: Journal of Cell Science, The Company of Biologists, Vol. 104, No. 2 ( 1993-02-01), p. 237-247
    Abstract: Cells from three layers of the bovine esophageal epithelium, representing different stages of differentiation, were dissociated and separated by Percoll gradient centrifugation into fractions of small, medium and large sizes. A majority of the large cells possessed condensed nuclei, a characteristic feature of terminal differentiation of the superficial epithelium. The small cells resembled the proliferate cells of the basal layer. In vitro culture of the esophageal epithelial cells resulted in proliferation of the small cells, colony formation, and, in some cases, differentiation into cells with condensed nuclei. Nuclei, or nuclear subfractions derived from cells of the different layers, were used as immunogens for the generation of hybridomas secreting monoclonal antibodies that bound specifically to different regions of the esophageal tissue. One such antibody, designated W2, labeled the condensed nuclei from the superficial layer of stratified esophageal and corneal epithelia in situ, as well as the large cells from esophageal culture in vitro. Thus, the expression of the W2 antigen may be associated with the process of nuclear condensation during epithelial differentiation. Immunoisolation of the target antigen of W2 from extracts of large cells of the bovine esophagus yielded a band of Mr ∼33,000 on nonreducing polyacrylamide gels. This band dissociated into two polypeptides, of Mr ∼22,000 and ∼11,000, upon treatment with dithiothreitol. Amino acid sequence analysis of the larger polypeptide showed extensive homology to a group of small calcium-binding proteins, including two helix-turn-helix motifs designated as the EF-hand, characteristic of the configuration of the metal-ion coordinating ligands of the calcium-binding site. Similarly, the sequence at the amino terminus of the polypeptide of ∼11,000 indicated that it was the light chain counterpart of the same calcium-binding protein complex.
    Type of Medium: Online Resource
    ISSN: 0021-9533 , 1477-9137
    URL: Article
    DOI: 10.1242/jcs.104.2.237
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 1993
    detail.hit.zdb_id: 219171-4
    detail.hit.zdb_id: 1483099-1
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Abstract 919: Intercalated Disk Protein Xin-beta is Required for the Hippo/YAP Signaling in the Heart
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Circulation Research Vol. 125, No. Suppl_1 ( 2019-08-02)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 125, No. Suppl_1 ( 2019-08-02)
    Abstract: Cardiovascular diseases continue to be a leading cause of death and disability. Despite this alarming fact, there is lack of effectual treatment and the molecular mechanisms underlying these devastating diseases remain elusive. Intercalated disk (ICD) is not only essential for the integrity of cardiomyocytes to withstand the strong mechanical forces imposed by constant heart beating; it is also critical for the dissemination of the electrical signal that initiates cardiac contraction. However, relatively less is known about how ICD transmits pathophysiological signals in cardiomyocytes to modulate gene expression and cardiac function. The Xin-α and Xin-β, belongs to a family of Xin-repeat containing proteins, are primarily located at the ICD of adult cardiomyocytes. They play an important role during heart development. Interestingly, the human homologue of the mouse Xin-β gene was mapped to a locus associated with cardiomyopathy; most importantly, mutations in Xin-α and Xin-β have been found in patients with cardiomyopathy, underscoring the importance of Xin genes to cardiac disease. Our previous studies have shown that Xin-β KO mice die postnatally with severe cardiomyopathy. Here, we report that loss of Xin-β results in defect in cardiomyocyte proliferation. Unbiased transcriptome analyses reveal that gene program related to the Hippo/Yap pathway is altered, leading to the hypothesis that Xin-β regulates cardiomyocyte proliferation and cardiac function by modulating the Hippo/Yap signaling. We identify physical and genetic interaction between Xin-β and components of the Hippo/Yap pathway. We further show that the expression of Xin-β is transcriptionally regulated by Mef2a, Yap and Tead1, suggesting the presence of a Xin-β/Yap feedback regulatory network in the heart. Strikingly, cardiac-specific overexpression of Yap markedly rescues cardiac defects in Xin-β KO mice; indicating a functional and genetic interaction between Xin-β and Yap. Together, our study reveals a novel molecular mechanism by which the ICD protein Xin-β modulates important pathophysiological Hippo/Yap signals to control heart development and cardiac function. Molecules uncovered here will become candidate targets for therapeutic treatment of cardiac disease.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.125.suppl_1.919
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 1467838-X
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  • 5
    Online Resource
    Online Resource
    Localization and function of Xinα in mouse skeletal muscle
    American Physiological Society ; 2013
    In:  American Journal of Physiology-Cell Physiology Vol. 304, No. 10 ( 2013-05-15), p. C1002-C1012
    Details
    In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 304, No. 10 ( 2013-05-15), p. C1002-C1012
    Abstract: The Xin repeat-containing proteins were originally found in the intercalated discs of cardiac muscle with implicated roles in cardiac development and function. A pair of paralogous genes, Xinα ( Xirp1) and Xinβ ( Xirp2), is present in mammals. Ablation of the mouse Xinα ( mXinα) did not affect heart development but caused late-onset adulthood cardiac hypertrophy and cardiomyopathy with conductive defects. Both mXinα and mXinβ are also found in the myotendinous junction (MTJ) of skeletal muscle. Here we investigated the structural and functional significance of mXinα in skeletal muscle. In addition to MTJ and the contact sites between muscle and perimysium, mXinα but not mXinβ was found in the blood vessel walls, whereas both proteins were absent in neuromuscular junctions and nerve fascicles. Coimmunoprecipitation suggested association of mXinα with talin, vinculin, and filamin, but not β-catenin, in adult skeletal muscle, consistent with our previous report of colocalization of mXinα with vinculin. Loss of mXinα in mXinα-null mice had subtle effects on the MTJ structure and the levels of several MTJ components. Diaphragm muscle of mXinα-null mice showed hypertrophy. Compared with wild-type controls, mouse extensor digitorum longus (EDL) muscle lacking mXinα exhibited no overt change in contractile and relaxation velocities or maximum force development but better tolerance to fatigue. Loaded fatigue contractions generated stretch injury in wild-type EDL muscle as indicated by a fragmentation of troponin T. This effect was blunted in mXinα-null EDL muscle. The results suggest that mXinα play a role in MTJ conductance of contractile and stretching forces.
    Type of Medium: Online Resource
    ISSN: 0363-6143 , 1522-1563
    URL: Article
    DOI: 10.1152/ajpcell.00005.2013
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2013
    detail.hit.zdb_id: 1477334-X
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Intercalated disc protein Xinβ is required for Hippo-YAP signaling in the heart
    Springer Science and Business Media LLC ; 2020
    In:  Nature Communications Vol. 11, No. 1 ( 2020-09-16)
    Details
    In: Nature Communications, Springer Science and Business Media LLC, Vol. 11, No. 1 ( 2020-09-16)
    Abstract: Intercalated discs (ICD), specific cell-to-cell contacts that connect adjacent cardiomyocytes, ensure mechanical and electrochemical coupling during contraction of the heart. Mutations in genes encoding ICD components are linked to cardiovascular diseases. Here, we show that loss of Xinβ, a newly-identified component of ICDs, results in cardiomyocyte proliferation defects and cardiomyopathy. We uncovered a role for Xinβ in signaling via the Hippo-YAP pathway by recruiting NF2 to the ICD to modulate cardiac function. In Xinβ mutant hearts levels of phosphorylated NF2 are substantially reduced, suggesting an impairment of Hippo-YAP signaling. Cardiac-specific overexpression of YAP rescues cardiac defects in Xinβ knock-out mice—indicating a functional and genetic interaction between Xinβ and YAP. Our study reveals a molecular mechanism by which cardiac-expressed intercalated disc protein Xinβ modulates Hippo-YAP signaling to control heart development and cardiac function in a tissue specific manner. Consequently, this pathway may represent a therapeutic target for the treatment of cardiovascular diseases.
    Type of Medium: Online Resource
    ISSN: 2041-1723
    URL: Article
    DOI: 10.1038/s41467-020-18379-8
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 2553671-0
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  • 7
    Online Resource
    Online Resource
    Isolation of a novel tropomyosin isoform from human colon cancer cell line T-84 and its expression in primary colon cancer and in ulcerative colitis (UC) mucosa
    Elsevier BV ; 2000
    In:  Gastroenterology Vol. 118, No. 4 ( 2000-4), p. A260-
    Details
    In: Gastroenterology, Elsevier BV, Vol. 118, No. 4 ( 2000-4), p. A260-
    Type of Medium: Online Resource
    ISSN: 0016-5085
    URL: Article
    DOI: 10.1016/S0016-5085(00)83114-5
    RVK:
    XA 44500
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2000
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  • 8
    Online Resource
    Online Resource
    Caldesmon mutant defective in Ca2+-calmodulin binding interferes with assembly of stress fibers and affects cell morphology, growth and motility
    The Company of Biologists ; 2004
    In:  Journal of Cell Science Vol. 117, No. 16 ( 2004-07-15), p. 3593-3604
    Details
    In: Journal of Cell Science, The Company of Biologists, Vol. 117, No. 16 ( 2004-07-15), p. 3593-3604
    Abstract: Despite intensive in vitro studies, little is known about the regulation of caldesmon (CaD) by Ca2+-calmodulin (Ca2+-CaM) in vivo. To investigate this regulation, a mutant was generated of the C-terminal fragment of human fibroblast CaD, termed CaD39-AB, in which two crucial tryptophan residues involved in Ca2+-CaM binding were each replaced with alanine. The mutation abolished most CaD39-AB binding to Ca2+-CaM in vitro but had little effect on in vitro binding to actin filaments and the ability to inhibit actin/tropomyosin-activated heavy meromyosin ATPase. To study the functional consequences of these mutations in vivo, we transfected an expression plasmid carrying CaD39-AB cDNA into Chinese hamster ovary (CHO) cells and isolated several clones expressing various amounts of CaD39-AB. Immunofluorescence microscopy revealed that mutant CaD39-AB was distributed diffusely throughout the cytoplasm but also concentrated at membrane ruffle regions. Stable expression of CaD39-AB in CHO cells disrupted assembly of stress fibers and focal adhesions, altered cell morphology, and slowed cell cycle progression. Moreover, CaD39-AB-expressing cells exhibited motility defects in a wound-healing assay, in both velocity and the persistence of translocation, suggesting a role for CaD regulation by Ca2+-CaM in cell migration. Together, these results demonstrate that CaD plays a crucial role in mediating the effects of Ca2+-CaM on the dynamics of the actin cytoskeleton during cell migration.
    Type of Medium: Online Resource
    ISSN: 1477-9137 , 0021-9533
    URL: Article
    DOI: 10.1242/jcs.01216
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2004
    detail.hit.zdb_id: 219171-4
    detail.hit.zdb_id: 1483099-1
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    1274 Full-Open Reading Frames of Transcripts Expressed in the Developing Mouse Nervous System
    Cold Spring Harbor Laboratory ; 2004
    In:  Genome Research Vol. 14, No. 10b ( 2004-10-15), p. 2053-2063
    Details
    In: Genome Research, Cold Spring Harbor Laboratory, Vol. 14, No. 10b ( 2004-10-15), p. 2053-2063
    Abstract: As part of the trans-National Institutes of Health (NIH) Mouse Brain Molecular Anatomy Project (BMAP), and in close coordination with the NIH Mammalian Gene Collection Program (MGC), we initiated a large-scale project to clone, identify, and sequence the complete open reading frame (ORF) of transcripts expressed in the developing mouse nervous system. Here we report the analysis of the ORF sequence of 1274 cDNAs, obtained from 47 full-length-enriched cDNA libraries, constructed by using a novel approach, herein described. cDNA libraries were derived from size-fractionated cytoplasmic mRNA isolated from brain and eye tissues obtained at several embryonic stages and postnatal days. Altogether, including the full-ORF MGC sequences derived from these libraries by the MGC sequencing team, NIH_BMAP full-ORF sequences correspond to ∼20% of all transcripts currently represented in mouse MGC. We show that NIH_BMAP clones comprise 68% of mouse MGC cDNAs ≥5 kb, and 54% of those ≥4 kb, as of March 15, 2004. Importantly, we identified transcripts, among the 1274 full-ORF sequences, that are exclusively or predominantly expressed in brain and eye tissues, many of which encode yet uncharacterized proteins.
    Type of Medium: Online Resource
    ISSN: 1088-9051
    URL: Article
    DOI: 10.1101/gr.2601304
    RVK:
    XA 10000
    Language: English
    Publisher: Cold Spring Harbor Laboratory
    Publication Date: 2004
    detail.hit.zdb_id: 1483456-X
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Discontinuous thoracic venous cardiomyocytes and heart exhibit synchronized developmental switch of troponin isoforms
    Wiley ; 2012
    In:  FEBS Journal ( 2012-12), p. n/a-n/a
    Details
    In: FEBS Journal, Wiley, ( 2012-12), p. n/a-n/a
    Type of Medium: Online Resource
    ISSN: 1742-464X
    URL: Article
    DOI: 10.1111/febs.12076
    Language: English
    Publisher: Wiley
    Publication Date: 2012
    detail.hit.zdb_id: 2172518-4
    SSG: 12
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