Showing papers by "University of California, San Francisco published in 1991"
TL;DR: The development and evaluation of a brief, multidimensional, self-administered, social support survey that was developed for patients in the Medical Outcomes Study (MOS), a two-year study of patients with chronic conditions is described.
5,617Β citations
TL;DR: GTPases are conserved molecular switches, built according to a common structural design, and rapidly accruing knowledge of individual GTPasesβcrystal structures, biochemical properties, or results of molecular genetic experimentsβsupport and generate hypotheses relating structure to function in other members of the diverse family of GTPase.
Abstract: GTPases are conserved molecular switches, built according to a common structural design. Rapidly accruing knowledge of individual GTPases--crystal structures, biochemical properties, or results of molecular genetic experiments--support and generate hypotheses relating structure to function in other members of the diverse family of GTPases.
3,236Β citations
TL;DR: A novel signaling mechanism in which thrombin cleaves its receptor's amino-terminal extension to create a new receptor amino terminus that functions as a tethered ligand and activates the receptor is revealed.
2,992Β citations
TL;DR: Cyclin degradation is the key step governing exit from mitosis and progress into the next cell cycle, and anaphase may be triggered by the recognition of cyclin by the ubiquitin-conjugating system.
Abstract: Cyclin degradation is the key step governing exit from mitosis and progress into the next cell cycle. When a region in the N terminus of cyclin is fused to a foreign protein, it produces a hybrid protein susceptible to proteolysis at mitosis. During the course of degradation, both cyclin and the hybrid form conjugates with ubiquitin. The kinetic properties of the conjugates indicate that cyclin is degraded by ubiquitin-dependent proteolysis. Thus anaphase may be triggered by the recognition of cyclin by the ubiquitin-conjugating system.
2,372Β citations
TL;DR: Understanding prion diseases may advance investigations of other neurodegenerative disorders and of the processes by which neurons differentiate, function for decades, and then grow senescent.
Abstract: Prions cause transmissible and genetic neurodegenerative diseases, including scrapie and bovine spongiform encephalopathy of animals and Creutzfeldt-Jakob and Gerstmann-Straussler-Scheinker diseases of humans. Infectious prion particles are composed largely, if not entirely, of an abnormal isoform of the prion protein, which is encoded by a chromosomal gene. A posttranslational process, as yet unidentified, converts the cellular prion protein into an abnormal isoform. Scrapie incubation times, neuropathology, and prion synthesis in transgenic mice are controlled by the prion protein gene. Point mutations in the prion protein genes of animals and humans are genetically linked to development of neuro-degeneration. Transgenic mice expressing mutant prion proteins spontaneously develop neurologic dysfunction and spongiform neuropathology. Understanding prion diseases may advance investigations of other neurodegenerative disorders and of the processes by which neurons differentiate, function for decades, and then grow senescent.
1,941Β citations
TL;DR: In this paper, the authors divide childhood trauma into two basic types and define the findings that can be used to characterize each of these types, including full, detailed memories, "omens," and misperceptions.
Abstract: Childhood psychic trauma appears to be a crucial etiological factor in the development of a number of serious disorders both in childhood and in adulthood. Like childhood rheumatic fever, psychic trauma sets a number of different problems into motion, any of which may lead to a definable mental condition. The author suggests four characteristics related to childhood trauma that appear to last for long periods of life, no matter what diagnosis the patient eventually receives. These are visualized or otherwise repeatedly perceived memories of the traumatic event, repetitive behaviors, trauma-specific fears, and changed attitudes about people, life, and the future. She divides childhood trauma into two basic types and defines the findings that can be used to characterize each of these types. Type I trauma includes full, detailed memories, "omens," and misperceptions. Type II trauma includes denial and numbing, self-hypnosis and dissociation, and rage. Crossover conditions often occur after sudden, shocking deaths or accidents that leave children handicapped. In these instances, characteristics of both type I and type II childhood traumas exist side by side. There may be considerable sadness. Each finding of childhood trauma discussed by the author is illustrated with one or two case examples.
1,805Β citations
TL;DR: It seems likely that most malignancies arise from the collaborative effects of dominant and recessive lesions, andumeration of the number of tumor suppressor genes afflicted in any given tumor may be greater.
1,643Β citations
TL;DR: Liposome formulations incorporating a synthetic polyethylene glycol-derivatized phospholipid can produce a large increase in the pharmacological efficacy of encapsulated antitumor drugs and have expanded considerably the prospects of liposomes as an effective carrier system for a variety of pharmacologically active macromolecules.
Abstract: The results obtained in this study establish that liposome formulations incorporating a synthetic polyethylene glycol-derivatized phospholipid have a pronounced effect on liposome tissue distribution and can produce a large increase in the pharmacological efficacy of encapsulated antitumor drugs. This effect is substantially greater than that observed previously with conventional liposomes and is associated with a more than 5-fold prolongation of liposome circulation time in blood, a marked decrease in uptake by tissues such as liver and spleen, and a corresponding increased accumulation in implanted tumors. These and other properties described here have expanded considerably the prospects of liposomes as an effective carrier system for a variety of pharmacologically active macromolecules.
1,640Β citations
TL;DR: The role of feedback controls in coordinating events in the cell cycle is discussed and the properties of mad mutants indicate that they are defective in the feedback control over the exit from mitosis are discussed.
1,252Β citations
TL;DR: The results demonstrate that the FGF signaling pathway plays an important role in early embryogenesis, particularly in the formation of the posterior and lateral mesoderm.
1,107Β citations
TL;DR: The similarity in response properties among the members of each class, their large, somatic "receptive fields," and the wide distribution of the terminal fields of axons of individual neurons to the trigeminal sensory complex and to multiple spinal segments indicate that these neurons exert a global influence over nociceptive responsiveness.
Abstract: Significant advances have been made in our understanding of nociceptive modulation from RVM. Among the most useful conceptually has been the discovery that there are two classes of modulatory neurons in the RVM that are likely to have opposing actions on nociception: on-cells, which may facilitate nociceptive transmission, and off-cells, which probably have a net inhibitory effect on nociception. The similarity in response properties among the members of each class, their large, somatic "receptive fields," and the wide distribution of the terminal fields of axons of individual neurons to the trigeminal sensory complex and to multiple spinal segments indicate that these neurons exert a global influence over nociceptive responsiveness. Drug microinjections into the RVM presumably shift the balance between states of on- or off-cell firing and also produce measurable changes in the threshold for nocifensor reflexes. The meaningful unit of function in the RVM nociceptive modulatory system therefore probably consists of large ensembles of physiologically and pharmacologically similar neurons. The strong coordination of activity of the two classes of RVM neuron may depend largely upon intranuclear projections from RVM off-cells that excite other off-cells and inhibit on-cells. The off-cell pause is GABA-mediated, and it is likely that there is a subset of GABA-containing RVM on-cells that directly inhibit off-cells. Furthermore, the available evidence indicates that exogenous opiates activate off-cells by inhibiting GABAergic release. Presumably, enkephalinergic cells in the RVM disinhibit off-cells in a similar way. Although non-serotonin-containing off-cells certainly exist, we propose that some off-cells contain serotonin. Other possible connections are based on more limited data; however, ACh, neurotensin, NE, and EAAs are present in neurons that project to the RVM, and each of these compounds, when microinjected into the RVM, has a modulating effect on nociceptive transmission. The local circuits in the RVM that underlie these actions remain to be elucidated. At the level of the dorsal horn, there is good evidence for each of three inhibitory mechanisms: direct inhibition of nociceptive projection neurons, inhibition of excitatory relay interneurons, and excitation of an inhibitory interneuron. The relative contribution made by each of these circuits is unknown.(ABSTRACT TRUNCATED AT 400 WORDS)
TL;DR: A visual analogue scale to evaluate fatigue severity (VAS-F) was developed and tested and demonstrated significant differences between their evening and morning scores, while sleep-disordered patients did not.
Abstract: A visual analogue scale to evaluate fatigue severity (VAS-F) was developed and tested in a sample of 75 healthy individuals and a sample of 57 patients undergoing medical evaluation for sleep disorders. The scale consists of 18 items related to fatigue and energy, has simple instructions, and is completed with minimal time and effort. The VAS-F compares favorably with the Stanford Sleepiness Scale and the Profile of Mood States, and its internal consistency reliabilities are high. Healthy subjects demonstrated significant differences between their evening and morning scores on the VAS-F, while sleep-disordered patients did not.
TL;DR: A complementary DNA clone containing the coding sequence of one of these rapidly responding channels, a 5HT3 subtype of the serotonin receptor, has been isolated by screening a neuroblastoma expression library for functional expression of serotonin-gated currents in Xenopus oocytes.
Abstract: The neurotransmitter serotonin (5HT) activates a variety of second messenger signaling systems and through them indirectly regulates the function of ion channels. Serotonin also activates ion channels directly, suggesting that it may also mediate rapid, excitatory responses. A complementary DNA clone containing the coding sequence of one of these rapidly responding channels, a 5HT3 subtype of the serotonin receptor, has been isolated by screening a neuroblastoma expression library for functional expression of serotonin-gated currents in Xenopus oocytes. The predicted protein product has many of the features shared by other members of the ligand-gated ion channel family. The pharmacological and electrophysiological characteristics of the cloned receptor are largely consistent with the properties of native 5HT3 receptors. Messenger RNA encoding this receptor is found in the brain, spinal cord, and heart. This receptor defines a new class of excitatory ligand-gated channels.
TL;DR: It is suggested that neuromuscular and cognitive impairment, as well as the circumstances of falls, affect the risk of injury when a fall occurs.
Abstract: We conducted a prospective study of the consequences of falls in 325 elderly community-dwelling persons, all of whom had fallen in the previous year. We contacted subjects every week for one year to ascertain falls and to determine the circumstances and consequences of falls. Only 6% of 539 falls resulted in a major injury (fracture, dislocation, or laceration requiring suture), but over half (55%) resulted in minor soft tissue injury. One in ten falls left the faller unable to get up for at least 5 minutes, and one in four falls caused subjects to limit their activities. The risk of injury per fall was about the same regardless of the number of falls a person had during follow-up. The risk of major injury was increased (age- and sex-adjusted odds ratio: 5.9, 95% confidence interval: 2.3-14.9) in falls associated with loss of consciousness compared to nonsyncopal falls. In multivariate analyses of nonsyncopal falls, the risk of major injury per fall was higher in persons having a previous fall with fracture (6.7; 2.1-21.5), a slower Trail Making B time (1.9; 1.1-3.2), and in Whites (18.4; 7.5-44.6). The risk that a nonsyncopal fall would result in minor injury (versus no injury) was increased in persons with a slower hand reaction time (1.8; 1.0-3.2) decreased grip strength (1.5; 1.0-2.3), in Whites (2.0; 1.0-3.7), in falls while using stairs and steps (2.2; 1.0-5.0), and turning around or reaching (3.5; 1.7-7.3). Our findings suggest that neuromuscular and cognitive impairment, as well as the circumstances of falls, affect the risk of injury when a fall occurs. Language: en
TL;DR: It is shown that brain-derived neurotrophic factor (BDNF) and NT-3, but not NGF, can induce rapid phosphorylation on tyrosine of gp 145trkB, one of the receptors encoded by trkB, indicating that gp145trkB may function as a neurotrophic receptor for BDNF andNT-3.
TL;DR: A potential role for MCP-1 in mediating monocytic infiltration of the artery wall is suggested, based on immunohistochemical staining of serial sections and on cell morphology.
Abstract: Monocytes appear to be central to atherogenesis both as the progenitors of foam cells and as a potential source of growth factors mediating intimal hyperplasia, but the chemical messages which stimulate the influx of monocytes into human atheroma remain unknown. Monocyte chemoattractant protein-1 (MCP-1) is a recently described molecule with powerful monocyte chemotactic activity expressed by monocytes, vascular endothelial cells, and smooth muscle cells in culture. To begin to address the role of MCP-1 in vivo, we examined 10 normal arteries and 14 diseased human arteries for MCP-1 expression by in situ hybridization. MCP-1 mRNA was detected in 16% of 10,768 cells counted in human carotid endarterectomy specimens with highest expression seen in organizing thrombi (33%) and in macrophage rich areas bordering the necrotic lipid core (24%) as compared to the fibrous cap (8%) and the necrotic lipid core itself (5%). Based on immunohistochemical staining of serial sections and on cell morphology, MCP-1 mRNA appeared to be expressed by vascular smooth muscle cells (VSMC), mesenchymal appearing intimal cells (MICs), and macrophages. By contrast, few cells expressing MCP-1 mRNA were found in normal arteries (less than 0.1%). These data suggest a potential role for MCP-1 in mediating monocytic infiltration of the artery wall.
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TL;DR: The chapter discusses the methods for preparing and utilizing frog cell cycle extracts and the fluctuation of MPF activity in early Xenopus embryos.
Abstract: Publisher Summary This chapter reviews the early Xenopus cycle and the history of cell cycle extracts. The early Xenopus cell cycles are controlled by the activation and inactivation of a protein kinase named maturation-promoting factor (MPF). MPF is also known as the cdc2 kinase and growth-associated histone H1 kinase, and consists of two principal subunits, the catalytic p34cdc2 subunit and cyclin. Activation of MPF induces both mitosis and meiosis, whereas its inactivation triggers the onset of anaphase and the progression into interphase. The fluctuation of MPF activity in early Xenopus embryos is discussed in the chapter. The chapter discusses the methods for preparing and utilizing frog cell cycle extracts. Female frogs are primed for ovulation by injecting them with pregnant mare serum gonadotropin (PMSG) and then induced to ovulate by a subsequent injection of human chorionic gonadotropin (HCG). The chapter also describes sperm nucleus preparation.
TL;DR: The development of synthetic, peptide and protein fragment models of the denatured state and the recent progress in NMR spectroscopy provide bases for optimism that new insights will be gained into this poorly understood realm of protein biochemistry.
Abstract: The denatured "state" of a protein is a distribution of many different molecular conformations, the averages of which are measured by experiments. The properties of this ensemble depend sensitively on the solution conditions. There is now considerable evidence that even in strong denaturants such as 6M GuHC1 and 9M urea, some structure may remain in protein chains. Under milder or physiological conditions, the denatured states of most proteins appear to be highly compact with extensive secondary structure. Both theoretical and experimental studies suggest that hydrophobic interactions, chain conformational entropies, and electrostatic forces are dominant in determining this structure. The denaturation reaction of many proteins in GuHC1 or urea can be most simply modelled as a two-state transition between the native structure and a relatively compact denatured state, which then undergoes a gradual increase in radius on further addition of denaturant. However, when a protein acquires a large net charge in acids or bases, it can have two stable denatured populations, one compact and the other more highly unfolded. The prediction and elucidation of the structural details of the non-native states of proteins may ultimately prove to be as difficult as predicting the native structures, particularly for D0, the denatured state under physiological conditions. Just as with the native state, the structure of this biologically important denatured state appears to depend on the amino acid sequence. The development of synthetic, peptide and protein fragment models of the denatured state and the recent progress in NMR spectroscopy provide bases for optimism that new insights will be gained into this poorly understood realm of protein biochemistry.
TL;DR: It is found that the cdc25 sequence shows weak but significant homology to a phylogenetically diverse group of protein tyrosine phosphatases, and is a specific protein phosphatase that dephosphorylates tyrosines and possibly threonine residues on p34cdc2 and regulates MPF activation.
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TL;DR: The ability to detect lying was evaluated in 509 people including law-enforcement personnel, such as members of the U.S. Secret Service, Central Intelligence Agency, Federal Bureau of Investigation, National Security Agency, Drug Enforcement Agency, California police and judges, as well as psychiatrists, college students, and working adults.
Abstract: The ability to detect lying was evaluated in 509 people including law-enforcement personnel, such as members of the US Secret Service, Central Intelligence Agency, Federal Bureau of Investigation, National Security Agency, Drug Enforcement Agency, California police and judges, as well as psychiatrists, college students, and working adults A videotape showed 10 people who were either lying or telling the truth in describing their feelings Only the Secret Service performed better than chance, and they were significantly more accurate than all of the other groups When occupational group was disregarded, it was found that those who were accurate apparently used different behavioral clues and had different skills than those who were inaccurate
TL;DR: In goldfish epithelial keratocytes, the actin microfilaments in the lamellipodium remain approximately fixed relative to the substrate as the cell moves over them, regardless of cell speed.
Abstract: The dynamic behaviour of actin filaments has been directly observed in living, motile cells using fluorescence photoactivation. In goldfish epithelial keratocytes, the actin microfilaments in the lamellipodium remain approximately fixed relative to the substrate as the cell moves over them, regardless of cell speed. The rate of turnover of actin subunits in the lamellipodium is remarkably rapid. Cell movement is directly and tightly coupled to the formation of new actin filaments at the leading edge.
TL;DR: Data indicate that CD8/zeta can activate the appropriate signal transduction pathways in the absence of CD3 gamma, delta, and epsilon, and suggest that the role ofCD3 zeta is to couple the TCR to intracellular signal transduct mechanisms.
TL;DR: This review focuses on cellular and molecular themes not emphasized in the previous one and includes examples of recent work on nonneural systems that illustrate probable future directions for research in the nervous system.
Abstract: The development of neurons and virtually all other cell types in the organism depends upon interactions with molecules in their environment. Studics of individual cell types have revealed tremendous diversity in the molecules that regulate the development of cells in the nervous system. These include chemotropic and trophic factors [e.g. nerve growth-factor (NGF) and brain derived neurotrophic factor (BDNF)], cell adhesion molecules [e.g. the neural cell adhesion molecule (NCAM) and N-cadherin], and molecules secreted into the extracellular matrix (ECM) [e.g. laminin (LN) and fibronectin (FN)]. Each class of molecule has now been shown to influence major steps in the development of the nervous system, including neuronal survival, determination, and migration; axonal growth and guidance; synapse formation; and glial differentiation. As molecules in the ECM influence all of these events and can be used to illustrate many of the principles derived from studies of the other classes of molecules, this review focuses upon constituents of the ECM and their receptors. The role of the ECM in neural development has recently been reviewed in this series (Sanes 1989). This review focuses on cellular and molecular themes not emphasized in the previous one and includes examples of recent work on nonneural systems that illustrate probable future directions for research in the nervous system.
Recent reviews on the composition and function of the ECM and its receptors include those of Hynes (1990), Hemler (1990), Kishimoto et al (1989), Plow & Ginsberg (1989), Burgeson (1988), Buck & Horowitz (1987), McDonald (1988), Ruoslahti (1988, 1989), Fessler & Fessler (1989), and Erickson & Bourdon (1989). Reviews focusing on aspects of ECM function in neural development include those by Lander (1989), Sanes (1989), and Edgar (1989). Because of space limitations, only representative examples and references are cited in this review.
TL;DR: It is concluded that the 92-kD type IV collagenase is critical for cytotrophoblast invasion, whereas inhibitors of the plasminogen activator system had only a partial inhibitory effect.
Abstract: The specialized interaction between embryonic and maternal tissues is unique to mammalian development. This interaction begins with invasion of the uterus by the first differentiated embryonic cells, the trophoblasts, and culminates in formation of the placenta. The transient tumor-like behavior of cytotrophoblasts, which peaks early in pregnancy, is developmentally regulated. Likewise, in culture only early-gestation human cytotrophoblasts invade a basement membrane-like substrate. These invasive cells synthesize both metalloproteinases and urokinase-type plasminogen activator. Metalloproteinase inhibitors and a function-perturbing antibody specific for the 92-kD type IV collagen-degrading metalloproteinase completely inhibited cytotrophoblast invasion, whereas inhibitors of the plasminogen activator system had only a partial (20-40%) inhibitory effect. We conclude that the 92-kD type IV collagenase is critical for cytotrophoblast invasion.
TL;DR: The accuracy of Gordon Holmes' retinotopic map of human striate cortex was tested by correlating magnetic resonance scans with homonymous field defects in patients with clearly defined occipital lobe lesions as mentioned in this paper.
Abstract: We have tested the accuracy of Gordon Holmes' retinotopic map of human striate cortex by correlating magnetic resonance scans with homonymous field defects in patients with clearly defined occipital lobe lesions. Our findings indicate that Holmes underestimated the cortical magnification of central vision. In a revised map of the human striate cortex, we expand the area subserving central vision and reduce the area devoted to peripheral vision. These changes bring the map of human striate cortex into agreement with data reported for closely related nonhuman primate species.
TL;DR: The combination of epidemiological studies with demonstration of physiological changes with exposure to ETS, together with biochemical evidence that elements of ETS have significant adverse effects on the cardiovascular system, leads to the conclusion that ETS causes heart disease.
Abstract: The evidence that ETS increases risk of death from heart disease is similar to that which existed in 1986 when the US Surgeon General concluded that ETS caused lung cancer in healthy nonsmokers. There are 10 epidemiological studies, conducted in a variety of locations, that reflect about a 30% increase in risk of death from ischemic heart disease or myocardial infarction among nonsmokers living with smokers. The larger studies also demonstrate a significant dose-response effect, with greater exposure to ETS associated with greater risk of death from heart disease. These epidemiological studies are complemented by a variety of physiological and biochemical data that show that ETS adversely affects platelet function and damages arterial endothelium in a way that increases the risk of heart disease. Moreover, ETS, in realistic exposures, also exerts significant adverse effects on exercise capability of both healthy people and those with heart disease by reducing the body's ability to deliver and utilize oxygen. In animal experiments, ETS also depresses cellular respiration at the level of mitochondria. The polycyclic aromatic hydrocarbons in ETS also accelerate, and may initiate, the development of atherosclerotic plaque. Of note, the cardiovascular effects of ETS appear to be different in nonsmokers and smokers. Nonsmokers appear to be more sensitive to ETS than do smokers, perhaps because some of the affected physiological systems are sensitive to low doses of the compounds in ETS, then saturate, and also perhaps because of physiological adaptions smokers undergo as a result of long-term exposure to the toxins in cigarette smoke. In any event, these findings indicate that, for cardiovascular disease, it is incorrect to compute "cigarette equivalents" for passive exposure to ETS and then to extrapolate the effects of this exposure on nonsmokers from the effects of direct smoking on smokers. These results suggest that heart disease is an important consequence of exposure to ETS. The combination of epidemiological studies with demonstration of physiological changes with exposure to ETS, together with biochemical evidence that elements of ETS have significant adverse effects on the cardiovascular system, leads to the conclusion that ETS causes heart disease. This increase in risk translates into about 10 times as many deaths from ETS-induced heart disease as lung cancer; these deaths contribute greatly to the estimated 53,000 deaths annually from passive smoking. This toll makes passive smoking the third leading preventable cause of death in the United States today, behind active smoking and alcohol.
TL;DR: It is shown here that a related 66 kd kinase, called mik1, acts redundantly with wee1 in the negative regulation of cdc2 in S, both in strains undergoing mitotic lethality and in those that are viable owing to a compensating mutation within cDC2.
TL;DR: Further elucidation of the molecular architecture and interactions of lipid and nonlipid components of the stratum corneum intercellular domains will be a prerequisite for a comprehensive understanding of stratum Corneum function.
Abstract: Publisher Summary This chapter discusses the structural and lipid biochemical correlates of the epidermal permeability barrier. A pivotal point in terrestrial adaptation is prevention of desiccation and maintenance of internal water homeostasis. The outermost integumentary tissue, the epidermis, maintains a reserve of germinal cell layers whose proliferation, stratification, and differentiation result in the production of the outermost layer, the anucleate stratum corneum. The stratum corneum has heterogeneous tissue structure possessing a selected array of enzymatic activity. The sequestration of lipids to intercellular domains and their organization into a unique multilamellar system have broad implications for permeability barrier function, water retention, desquamation, and percutaneous drug delivery. Yet, the functions and organization of specific lipid species in this membrane system are still unknown. Further, elucidation of the molecular architecture and interactions of lipid and nonlipid components of the stratum corneum intercellular domains will be a prerequisite for a comprehensive understanding of stratum corneum function.
TL;DR: St Stimulation of CD28, a molecule expressed on most human T cells, induced the formation of a protein complex that bound to a site on the IL-2 gene distinct from previously described binding sites and increasedIL-2 enhancer activity fivefold.
Abstract: The mechanism by which cell surface molecules regulate T cell production of lymphokines is poorly understood. Production of interleukin-2 (IL-2) can be regulated by signal transduction pathways distinct from those induced by the T cell antigen receptor. Stimulation of CD28, a molecule expressed on most human T cells, induced the formation of a protein complex that bound to a site on the IL-2 gene distinct from previously described binding sites and increased IL-2 enhancer activity fivefold. The CD28-responsive complex bound to the IL-2 gene between -164 and -154 base pairs from the transcription start site. The sequence of this element is similar to regions conserved in the 5' flanking regions of several other lymphokine genes.
TL;DR: The complementary DNA sequence was determined for the 92-kilodalton beta catenin of Xenopus laevis, a protein of desmosomal and zonula adherens cell junctions, and to the plakoglobin homolog in Drosophila melanogaster, the product of the segment polarity gene armadillo.
Abstract: Three cytoplasmic proteins, called catenins, bind to the cytoplasmic tail of the epithelial cell-cell adhesion molecule E-cadherin. The complementary DNA sequence was determined for the 92-kilodalton beta catenin of Xenopus laevis. The sequence is homologous to mammalian plakoglobin, a protein of desmosomal and zonula adherens cell junctions, and to the plakoglobin homolog in Drosophila melanogaster, the product of the segment polarity gene armadillo. A monoclonal antibody to bovine plakoglobin recognizes the analogous beta catenin in the Madin-Darby canine kidney (MDCK) cell line. Armadillo plakoglobin may link E-cadherin to the underlying actin cytoskeleton at cell-cell junctions; the E-cadherin-catenin protein complex may also participate in the transmission of developmental information.