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  • 1
    Electronic Resource
    Electronic Resource
    Thyroxine-induced gill resorption in the axolotl (ambystoma mexicanum)Supported in part by a grant from the University of Connecticut Research Foundation and General Research Support for the University of Connecticut Health Center from the National Institutes of Health, Bethesda, Maryland. (1977)
    New York, NY : Wiley-Blackwell
    Journal of Morphology 153 (1977), S. 479-503 
    Details
    ISSN: 0362-2525
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Normal gill structure and thyroxine induced resorptive changes were studied in Ambystoma mexicanum. The gill is normally composed of a mesenchymal core covered with a multilayered epithelium. The general architecture is simpler than that of the teleost and elasmobranch, but the vascular arrangement is analogous. There are three basic cell types in the epithelium: a characteristic epithelial cell containing tonofibrils and mucus, a ciliated cell with an ultrastructure similar to that of the chloride cell, and the mucin-filled Leydig cell. The basal lamella and mesenchymal tissue appear typical of amphibians.Cytologic changes during thyroxine induced gill resorption varied with cell type. Some epithelial cells demonstrated a cytoplasmic response with swelling of mitochondria and rough endoplasmic reticulum and late, lytic nuclear changes, while others remained viable and went on to cornify. Ciliated cells showed early changes in nuclear chromatin pattern followed by rapid, progressive dilatation of endoplasmic reticulum. Leydig cells sustained variable changes leading to collapse of the perinuclear mucus, and cells of this type were absent in mature epidermis. Early basement membrane changes included widening and reduplication of the adepidermal membrane followed by morphologic fraying of collagen plies. There is no cytologic evidence to suggest that autolysis plays a major role in gill tissue dissolution.Resorption involved the maintenance of structural integrity in the face of diminishing physical dimensions. The epithelium became cornified, the basement lamellae dissolved, and the mesenchymal tissue was resorbed through action of macrophages in an orderly distal to proximal direction.
    Additional Material: 3 Tab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jmor.1051530311
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  • 2
    Electronic Resource
    Electronic Resource
    Endoplasmic microtubules connect the advancing nucleus to the tip of legume root hairs, but F-actin is involved in basipetal migration (1987)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 8 (1987), S. 27-36 
    Details
    ISSN: 0886-1544
    Keywords: nuclear migration ; microtubules ; F-actin ; root hairs ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: A prominent feature of tip growth in filamentous plant cells is that the nucleus often migrates in step with the tip as it extends. We have studied this long-recognized but unexplained relationship in root hairs of the legume Vicia hirsuta by a variety of microscopic techniques. Using rhodaminyl lysine phallotoxin, and antitubulin antibodies, root hairs are shown to contain axial bundles of F-actin and a complex microtubular system. To the basal side of the nucleus the microtubules are cortical and net axial but in the region between nucleus and tip the arrangement is more complicated. Electron microscopic thin sections demonstrate that internal bundles of microtubles exist in addition to the plasma membrane-associated kind. Computerized deblurring of through-focal series of antitubulin stained hairs clarifies the three-dimensional organization: bundles of endoplasmic microtubules progress from the nuclear region toward the apical dome where they can be seen to fountain out upon the cortex.The relationship between nucleus and tip can be uncoupled with antimicrotubule herbicides. Time lapse video microscopy shows that these agents cause the nucleus to migrate toward the base. This contrary migration can be inhibited by adding cytochalasin D, which fragments the F-actin bundles.It is concluded that microtubules connect the nucleus to the tip but that F-actin is involved in basipetal migration as is known to occur when symbiotic bacteria uncouple the nucleus from the tip.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970080105
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  • 3
    Electronic Resource
    Electronic Resource
    Interaction of the insulin receptor kinase with serine/threonine kinases in vitro (1985)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 28 (1985), S. 171-182 
    Details
    ISSN: 0730-2312
    Keywords: insulin receptor ; tyrosine phosphorylation ; serine kinases ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Insulin causes rapid phosphorylation of the β subunit (Mr = 95,000) of its receptor in broken cell preparations. This occurs on tyrosine residues and is due to activation of a protein kinase which is contained in the receptor itself. In the intact cell, insulin also stimulates the phosphorylation of the receptor and other cellular proteins on serine and threonine residues. In an attempt to find a protein that might link the receptor tyrosine kinase to these serine/threonine phosphorylation reactions, we have studied the interaction of a partially purified preparation of insulin receptor with purified preparations of serine/threoine kinases known to phosphorylate glycogen synthase. No insulin-dependent phosphorylation was ob served when casein kinases I and II, phosphorylase kinase, or glycogen synthase kinase 3 was incubated in vitro with the insulin receptor. These kinases also failed to phosphorylate the receptor. By contrast, the insulin receptor kinase catalyzed the phosphorylation of the calmodulin-dependent kinase and addition of insulin in vitro resulted in a 40% increase in this phosphorylation. In the presence of calmodulin-dependent kinase and the insulin receptor kinase, insulin also stimulated the phosphorylation of calmodulin. Phosphoamino acid analysis showed an increase of phosphotyrosine content in both calmodulin and calmodulindependent protein kinase. These data suggest that the insulin receptor kinase may interact directly and specifically with the calmodulin-dependent kinase and calmodulin. Further studies will be required to determine if these phosphorylations modify the action of these regulatory proteins.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240280209
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  • 4
    Electronic Resource
    Electronic Resource
    Regulation of tissue transglutaminase gene expression as a molecular model for retinoid effects on proliferation and differentiation (1989)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 39 (1989), S. 293-304 
    Details
    ISSN: 0730-2312
    Keywords: retinoic acid ; transcriptional control ; antiproliteratiory differentiation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Retinoids (structural and functional analogs of vitamin A) are potent antiproliferative agents whose mode of action is poorly understood. It has been suggested that the molecular events that underscore their action involve alterations in gene expression, but no gene has yet been shown to be directly regulated by these molecules. Several years ago, we found that retinoic acid caused an accumulation of the enzyme tissue transglutaminase in murine peritoneal macrophages and in human promyelocytic leukemia (HL-60) cells. We now report that this induction is caused by an increase in the mRNA for this enzyme. Retinoic acid is the only mediator of this induction, since its effects do not depend on the presence of serum proteins. The induction of tissue transglutaminase mRNA is not due to an increase in its stability but to an increase in the relative transcription rate of its gene. We present a model to correlate the retinoid induction of tissue transglutaminase with retinoid effects on cellular growth and differentiation.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240390309
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  • 5
    Electronic Resource
    Electronic Resource
    Expression of basic helix-loop-helix transcription factors in explant hematopoietic progenitors (1996)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 61 (1996), S. 478-488 
    Details
    ISSN: 0730-2312
    Keywords: basic helix-loop-helix ; interleukin-1 ; interleukin-3 ; granulocyte-macrophage colony-stimulating factor ; progenitor ; transcription factor ; c-kit ligand ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The basic helix-loop-helix (bHLH) transcription factors form heterodimers and control steps in cellular differentiation. We have studied four bHLH transcription factors, SCL, lyl-1, E12/E47, and Id-1, in individual lineage-defined progenitors and hematopoietic growth factor - dependent cell lines, evaluating mRNA expression and the effects of growth factors and cell cycle phase on this expression. Single lineage-defined progenitors selected from early murine colony starts and grown under permissive conditions were analyzed by RT-PCR. SCL and E12/E47 were expressed in the vast majority of tri-, bi-, and unilineage progenitors of erythroid, macrophage, megakaryocyte, and neutrophil lineages. Expression for E12/E47 was not seen in unilineage megakaryocyte and erythroid or bilineage neutrophil/mast cell progenitors. Lyl-1 showed a more restricted pattern of expression, although expression was seen in some bi- and unilineage progenitors. No expression was detected in erythroid, erythroid-megakaryocyte-macrophage, macrophage-neutrophil, macrophage, or megakaryocytic progenitors. Id-1, an inhibitory bHLH transcription factor, was also widely expressed in all bi- and unilineage progenitors; only the trilineage erythroid-megakaryocyte-macrophage progenitors failed to show expression. Expression of these factors within a progenitor class was generally heterogeneous, with some progenitors showing expression and some not. This was seen even when two sister cells from the same colony start were analyzed. Id-1, but not E12/E47, mRNA was increased in FDC-P1 and MO7E hematopoietic cell lines after exposure to IL-3 or GM-CSF, Id-1, E12, and lyl-1 showed marked variation at different points in cell cycle in isoleucine-synchronized FDC-P1 cells. These results suggest that SCL, lyl-1, E12/E47, and Id-1 are important in hematopoietic progenitor cell regulation, and that their expression in hematopoietic cells varies in response to cytokines and/or during transit through cell cycle. © 1996 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
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  • 6
    Electronic Resource
    Electronic Resource
    Cell cycle-dependent modifications in activities of pRb-related tumor suppressors and proliferation-specific CDP/cut homeodomain factors in murine hematopoietic progenitor cells (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 66 (1997), S. 512-523 
    Details
    ISSN: 0730-2312
    Keywords: cell cycle control ; H4 gene promoter ; G1/S phase transition point ; CDP/cut ; interferon regulatory factor 2 ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The histone H4 gene promoter provides a paradigm for defining transcriptional control operative at the G1/S phase transition point in the cell cycle. Transcription of the cell cycle-dependent histone H4 gene is upregulated at the onset of S phase, and the cell cycle control element that mediates this activation has been functionally mapped to a proximal promoter domain designated Site II. Activity of Site II is regulated by an E2F-independent mechanism involving binding of the oncoprotein IRF2 and the multisubunit protein HiNF-D, which contains the homeodomain CDP/cut, CDC2, cyclin A, and the tumor suppressor pRb. To address mechanisms that define interactions of Site II regulatory factors with this cell cycle control element, we have investigated these determinants of transcriptional regulation at the G1/S phase transition in FDC-P1 hematopoietic progenitor cells. The representation and activities of histone gene regulatory factors were examined as a function of FDC-P1 growth stimulation. We find striking differences in expression of the pRb-related growth regulatory proteins (pRb/p105, pRb2/p130, and p107) following the onset of proliferation. pRb2/p130 is present at elevated levels in quiescent cells and declines following growth stimulation. By contrast, pRb and p107 are minimally represented in quiescent FDC-P1 cells but are upregulated at the G1/S phase transition point. We also observe a dramatic upregulation of the cellular levels of pRb2/p130-associated protein kinase activity when S phase is initiated. Selective interactions of pRb and p107 with CDP/cut are observed during the FDC-P1 cell cycle and suggest functional linkage to competency for DNA binding and/or transcriptional activity. These results are particularly significant in the context of hematopoietic differentiation where stringent control of the cell cycle program is requisite for expanding the stem cell population during development and tissue renewal. J. Cell. Biochem. 66:512-523, 1997. © 1997 Wiley-Liss, Inc.
    Additional Material: 6 Ill.
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  • 7
    Electronic Resource
    Electronic Resource
    The role of digital rectal examination, transrectal ultrasound, and prostate specific antigen for the detection of confined and clinically relevant prostate cancer (1992)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 50 (1992), S. 69-73 
    Details
    ISSN: 0730-2312
    Keywords: DRE ; predicted cancer volume ; prostate cancer ; PSA ; TRUS ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: In a study population, can digital rectal examination (DRE), transrectal ultrasound (TRUS), and prostate specific antigen (PSA) (monoclonal) effectively detect the majority of clinically relevant cancer? If this is possible, the remaining patients could then be considered for chemopreventive protocols.The American Cancer Society/National Prostate Cancer Detection Project (ACS/NPCDP) had a cancer detection rate of 2.4% for its initial year utilizing PSA, DRE and TRUS. TRUS and PSA detected 73% more cancer than DRE alone. TRUS detected a greater percentage of cancers than DRE (85% vs. 64%).PSA was ≥ 4 ng/ml for 66% of prostate cancer patients; 11% of cancer patients had PSA 〈 2 ng/ml. PSA decision levels based on gland volume detected a subgroup at the 95th percentile that had a nine-fold increased risk for cancer. In a separate study differentiating benign prostatic hypertrophy (BPH) and cancer, we found 0.12±0.13 ng/ml/gm for serum PSA (sPSA)/gm BPH. This study proved that predicted PSA (pPSA) = gland volume × 0.12; this equation also functioned at the 95th percentile for any individual patient.Individual patient assessment: 1Entry level PSA = 2 ng/ml.2Those patients with PSA 〉 2 ng/ml have TRUS determination of gland volume (performed by technician).3pPSA = gland volume × 0.12. If sPSA 〉 pPSA then:4(sPSA-pPSA)/2 = predicted volume (cc) of cancer;53√ volume of cancer = mean diameter (cm) of cancer.Thus, these results should detect the majority of clinically relevant cancer (〉0.5cc). PSA combined with TRUS and DRE can identify high risk groups for cancer. © 1992 Wiley-Liss, Inc.
    Additional Material: 4 Tab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240501216
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  • 8
    Electronic Resource
    Electronic Resource
    Function of osteocytes in bone (1994)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 55 (1994), S. 287-299 
    Details
    ISSN: 0730-2312
    Keywords: osteocyte ; gap junction ; cytoskeleton ; extracellular matrix ; osteocytic osteolysis ; bone membrane ; functional adaptation ; mechanical loading ; strain ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Although the structural design of cellular bone (i.e., bone containing osteocytes that are regularly spaced throughout the bone matrix) dates back to the first occurrence of bone as a tissue in evolution, and although osteocytes represent the most abundant cell type of bone, we know as yet little about the role of the osteocyte in bone metabolism. Osteocytes descend from osteoblasts. They are formed by the incorporation of osteoblasts into the bone matrix. Osteocytes remain in contact with each other and with cells on the bone surface via gap junction-coupled cell processes passing through the matrix via small channels, the canaliculi, that connect the cell body-containing lacunae with each other and with the outside world. During differentiation from osteoblast to mature osteocyte the cells lose a large part of their cell organelles. Their cell processes are packed with microfilaments. In this review we discuss the various theories on osteocyte function that have taken in consideration these special features of osteocytes. These are (1) osteocytes are actively involved in bone turnover; (2) the osteocyte network is through its large cell-matrix contact surface involved in ion exchange; and (3) osteocytes are the mechanosensory cells of bone and play a pivotal role in functional adaptation of bone. In our opinion, especially the last theory offers an exciting concept for which some biomechanical, biochemical, and cell biological evidence is already available and which fully warrants further investigations. © 1994 Wiley-Liss, Inc.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240550304
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  • 9
    Electronic Resource
    Electronic Resource
    Molecular physiology of the islet amyloid polypeptide (IAPP)/amylin gene in man, rat, and transgenic mice (1994)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 55 (1994), S. 39-53 
    Details
    ISSN: 0730-2312
    Keywords: CALC gene family ; genomic organization ; transcription regulation ; biosynthesis ; islet β-cell ; insulin resistance ; islet amyloid ; type 2 diabetes mellitus ; animal model ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Islet amyloid polypeptide (“amylin”) is the major protein component of amyloid deposits in pancreatic islets of type 2 (non-insulin-dependent) diabetic patients. Islet amyloid polypeptide consists of 37 amino acids, is co-produced and co-secreted with insulin from islet β-cells, can act as a hormone in regulation of carbohydrate metabolism, and is implicated in the pathogenesis of islet amyloid formation and of type 2 diabetes mellitus. Rat islet amyloid polypeptide differs from human islet amyloid polypeptide particularly in the region of amino acids 25-28, which is important for amyloid fibril formation. In rat and mouse, diabetes-associated islet amyloid does not develop. To study the genetic organization and biosynthesis of islet amyloid polypeptide, we have isolated and analyzed the human and rat islet amyloid polypeptide gene and corresponding cDNAs. Both genes contain 3 exons, encoding precursor proteins of 89 amino acids and 93 amino acids, respectively. Apart from a putative signal sequence, these precursors contain amino- and carboxy-terminal flanking peptides in addition to the mature islet amyloid polypeptide. To understand regulation of islet amyloid polypeptide gene expression, we have identified several potential cis-acting transcriptional control elements that influence β-cell-specific islet amyloid polypeptide gene expression. Using antisera raised against synthetic human islet amyloid polypeptide we developed a specific and sensitive radioimmunoassay to measure levels of islet amyloid polypeptide in plasma and tissue extracts. Also antisera raised against the flanking peptides will be used in studying human islet amyloid polypeptide biosynthesis. Elevated plasma islet amyloid polypeptide levels have been demonstrated in some diabetic, glucose-intolerant, and obese individuals, as well as in rodent models of diabetes and obesity. To examine the potential role of islet amyloid polypeptide overproduction in the pathogenesis of islet amyloid formation and type 2 diabetes, we generated transgenic mice that overproduce either the amyloidogenic human islet amyloid polypeptide or the nonamyloidogenic rat islet amyloid polypeptide in their islet β-cells. Despite moderately to highly (up to 15-fold) elevated plasma islet amyloid polypeptide levels, no marked hyperglycemia, hyperinsulinemia or obesity was observed. This suggests that chronic overproduction of islet amyloid polypeptide “per se” does not cause insulin resistance. No islet amyloid deposits were detected in mice up to 63 weeks of age, but in every mouse producing human islet amyloid polypeptide (as in man), accumulation of islet amyloid polypeptide was observed in β-cell lysosomal bodies. This may represent an initial phase in intracellular amyloid fibril formation. The human islet amyloid polypeptide overproducing transgenic mice model offers a unique opportunity to study the biosynthesis, intracellular handling, secretion, and extracellular handling of human islet amyloid polypeptide in vivo. © 1994 Wiley-Liss, Inc.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240550006
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  • 10
    Electronic Resource
    Electronic Resource
    POU-domain gene expression in the gastrointestinal tract (1995)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 58 (1995), S. 260-267 
    Details
    ISSN: 0730-2312
    Keywords: adaptation ; small bowel ; gut development ; homeogenes ; Oct-1 ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The process of self-renewal which occurs in the gastrointestinal epithelium is greatly amplified and accelerated during the intestinal adaptation which occurs in the residual ileum after massive small bowel resection (MSBR). As with growth and development, these processes must involve the coordinated regulation of many genes. Several families of nuclear proteins are known to be involved in the control of gene expression during development including the POU-domain genes; their expression has not been characterized in the gastrointestinal tract during normal cellular renewal or adaptation, and POU-domain encoding cDNAs were cloned from ileal RNA. Three known genes were cloned: Oct-1, Brn-1 and Tst-1 but no novel members of this gene family were identified. The encoded sequence for rat Oct-1 differs from that previously reported. Oct-1 is relatively ubiquitously expressed with increased expression during both development and adaptation. Minimal expression of Tst-1 was observed. Brn-1 exhibits limited expression in the adult gastrointestinal tract. but may play a role in the fetal gastrointestinal tract.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240580214
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