[Info] What's new in Nature
[Contents] [News and Views] 11 December 1997
Summaries of some of this week's stories
Experimental quantum teleportation
Quantum teleportation--the transmission and reconstruction over arbitrary distances of the state of a quantum system--is demonstrated experimentally. During teleportation, an initial photon which carries the polarization that is to be transferred and one of a pair of entangled photons are subjected to a measurement such that the second photon of the entangled pair acquires the polarization of the initial photon. This latter photon can be arbitrarily far away from the initial one. Quantum teleportation will be a critical ingredient for quantum computation networks.
D Bouwmeester, J-W Pan, K Mattle, M Eibl, H Weinfurter
& A Zeilinger

Experimental quantum teleportation (Article)
Nature 390, 575 (1997)
Genomic sequence of a Lyme disease spirochaete, Borrelia burgdorferi
The genome of the bacterium Borrelia burgdorferi B31, the aetiologic agent of Lyme disease, contains a linear chromosome of 910,725 base pairs and at least 17 linear and circular plasmids with a combined size of more than 533,000 base pairs. The chromosome contains 853 genes encoding a basic set of proteins for DNA replication, transcription, translation, solute transport and energy mEtabolism, but, like Mycoplasma genitalium, it contains no genes for cellular biosynthetic reactions. Because B. burgdorferi and M. genitalium are distantly related eubacteria, the authors suggest that their limited mEtabolic capacities reflect convergent evolution by gene loss from more mEtabolically competent progenitors. Of 430 genes on 11 plasmids, most have no known biological function; 39% of plasmid genes are paralogues that form 47 gene families. The biological significance of the multiple plasmid-encoded genes is not clear, although they may be involved in antigenic variation or immune evasion.
C M Fraser, S Casjens, W M Huang, G G Sutton, R Clayton, R Lathigra, O White, K A Ketchum, R Dodson, E K Hickey, M Gwinn, B Dougherty, J-F Tomb, R D Fleischmann, D Richardson, J Peterson, A R Kerlavage, J Quackenbush, S Salzberg, M Hanson, R van Vugt, N Palmer, M D Adams, J Gocayne, J Weidmann, T Utterback, L Watthey, L McDonald, P Artiach, C Bowman, S Garland, C Fujii, M D Cotton, K Horst, K Roberts, B Hatch, H O Smith & J C Venter
Genomic sequence of a Lyme disease spirochaete, Borrelia burgdorferi (Article)
Nature 390, 580 (1997)
Increasing X-ray emissions and periodic outbursts from the massive star Eta Carinae
Eta Carinae is one of the most massive, luminous and unstable stars known. The basic nature of this star is poorly understood, despite much study. It is a fluctuating source of hard X-rays, indicative of gas at an unusually high temperature (60 million kelvin): the mechanism for producing this gas has yet to be established, but may be related to strong shocks in a dense stellar wind. The authors have monitored the hard X-ray emission (2--10keV) from Eta Car over the past 1.5 years, in order to better understand the nature of these emissions and their variations. They show here that there has been an overall increase in the mean X-ray flux which has accelerated since January 1997, and that there are also small-scale periodic outbursts that occur every 85 days. It has recently been argued, that Eta Car is in fact a binary stellar system whose components are approaching periastron near 1 January 1998. If this is indeed the case, then it is plausible that the hard X-ray emission is produced by shocks associated with the collision of the winds from the two stars, in which case the X-ray flux should increase through periastron, and rapidly decline thereafter. Continued monitoring will test this prediction.
M F Corcoran, K Ishibashi, J H Swank, K Davidson, R Petre
& J H M M Schmitt

Increasing X-ray emissions and periodic outbursts from the massive star Eta Carinae (Letter to Nature)
Nature 390, 587 (1997)
Controlling the sign of quantum interference by tunnelling from quantum wells
The sign of the interference (constructive or destructive) between quantum-mechanical paths depends on the phase difference between the paths. In the Fano effect two optical paths from the ground state of a system--one direct and one mediated by a resonance--to a state in an energy continuum interfere to produce an asymmetric absorption spectrum that falls to zero near the absorption maximum. Zero absorption occurs as the wavelength is scanned across the resonance, at a photon energy corresponding to a 180 phase difference between the paths. Similar interference effects occur when two absorption paths are mediated by two different states, and they provide the basis for lasers that operate without a population inversion. Here the authors report the control, by quantum mechanical tunnelling, of interference in optical absorption. The two intermediate states are resonances that arise from the mixing of the states in two adjacent semiconductors quantum wells, which are broadened by tunnelling into the same energy continuum through an ultra-thin potential-energy barrier. Inverting the direction of tunnelling by reversing the position of the barrier with respect to the two quantum wells changes the interference from destructive to constructive, as predicted theoretically. This effect might provide a way to make semiconductor lasers without population inversion.
J Faist, F Capasso, C Sirtori, K W West & L N Pfeiffer
Controlling the sign of quantum interference by tunnelling from quantum wells (Letter to Nature)
Nature 390, 589 (1997)
Emergence of symbiosis in peptide self-replication through a hypercyclic network
Symbiosis is an association between different organisms that leads to a reciprocal enhancement of their ability to survive. Similar mutually beneficial relationships can operate at the molecular level in the form of a hypercycle, a collective of two or more self-replicating species interlinked through a cyclic catalytic network. The superposition of cross-catalysis onto autocatalytic replication integrates the members of the hypercycle into a single system that reproduces through a second-order (or higher) form of nonlinear autocatalysis. The hypercycle population as a whole is therefore able to compete more efficiently for existing resources than any one member on its own. In addition, the effects of beneficial mutations of any one member are spread over the entire population. The formation of hypercycles has been suggested as an important step in the transition from inanimate to living chemistry , and a large number of hypercycles are expected to be embedded within the complex networks of living systems. But only one naturally occurring hypercycle has been well documented, while two autocatalytic chemical systems may contain vestiges of hypercyclic organization. Here the authors report a chemical system that constitutes a clear example of a minimal hypercyclic network, in which two otherwise competitive self-replicating peptides symbiotically catalyse each others production.
D H Lee, K Severin, Y Yokobayashi & M R Ghadiri
Emergence of symbiosis in peptide self-replication through a hypercyclic network (Letter to Nature)
Nature 390, 591 (1997)
Kinetic limitations on droplet formation in clouds
The 'indirect' radiative cooling of climate due to the role of anthropogenic aerosols in cloud droplet formation processes (which affect cloud albedo) is potentially large, up to -1.5Wm-2. It is important to be able to determine the number concentration of cloud droplets to within a few per cent, as radiative forcing as a result of clouds is very sensitive to changes in this quantity, but empirical approaches are problematic. The initial growth of a subset of particles known as cloud condensation nuclei and their subsequent 'activation' to form droplets are generally calculated with the assumption that cloud droplet activation occurs as an equilibrium process described by classical Kohler theory. Here the authors show that this assumption can be invalid under certain realistic conditions. They conclude that the poor empirical correlation between cloud droplet and cloud condensation nuclei concentrations is partly a result of kinetically limited growth before droplet activation occurs. Ignoring these considerations in calculations of total cloud radiative forcing based on cloud condensation nuclei concentrations could lead to errors that are of the same order of magnitude as the total anthropogenic greenhouse-gas radiative forcing.
P Y Chuang, R J Charlson & J H Seinfeld
Kinetic limitations on droplet formation in clouds
(Letter to Nature)

Nature 390, 594 (1997)
Vanishing atomic migration barrier in SiO2
Understanding the high-pressure behaviour of SiO2, a prototypical network- forming material, is important for resolving many problems in the Earth sciences. For pressures of 1--3GPa (~1--3 104atm), it has been shown that increases in pressure result in higher rate constants for atomic transport processes such as diffusion, viscous flow and crystal growth in SiO2 as well as in some silicate melts. Structural transitions and coordination changes observed beyond 10GPa may also be related to this pressure-induced increase in atomic mobility. There must be limits, however, on the extent to which pressure can enhance mobility, as a migration barrier decreasing linearly with pressure should vanish at a critical pressure, beyond which a sudden change in behaviour should be observed. Here the authors report measurements of the pressure dependence of the growth rate of quartz from amorphous SiO2 for pressures up to 6GPa. They observe a sharp peak in growth rate--implying a minimum in viscosity--at 3GPa, which they interpret as evidence that the critical pressure is being traversed. The corresponding depth below the Earths surface at which this peak occurs (~100km) suggests that this critical pressure may be related to the ubiquitous cut-off in subduction-related volcanism observed when oceanic plates reach roughly this depth.
M J Aziz, S Circone & C B Agee
Vanishing atomic migration barrier in SiO2
(Letter to Nature)

Nature 390, 596 (1997)
Nonlinear ground-motion amplification by sediments during the 1994 Northridge earthquake
It has been known since at least 1898 that sediments can amplify earthquake ground motion relative to bedrock. For the weak ground motion accompanying small earthquakes, the amplification due to sediments is well understood in terms of linear elasticity (Hookes law), but there has been a long-standing debate regarding the amplification associated with the strong ground motion produced by large earthquakes. The view of geotechnical engineers, based largely on laboratory studies, is that Hookes law breaks down at larger strains causing a reduced (nonlinear) amplification. Seismologists, on the other hand, have tended to remain sceptical of this nonlinear effect, mainly because the relatively few strong-motion observations seemed to be consistent with linear elasticity. Although some recent earthquake studies have demonstrated nonlinear behaviour under certain circumstances, the significance of nonlinearity for the type of stiff-soil sites found in the greater Los Angeles region remains unresolved. Here the authors report that ground-motion amplification due to sediments for the main shock of the 1994 Northridge earthquake was up to a factor of two less than the amplification observed for its aftershocks. These observations imply significant nonlinearity in such amplification, and bring into question the use of measurements of weak ground motion to predict the strong ground motion at sedimentary sites.
E H Field, P A Johnson, I A Beresnev & Y Zeng
Nonlinear ground-motion amplification by sediments during the 1994 Northridge earthquake (Letter to Nature)
Nature 390, 599 (1997)
Absence of contour linking in peripheral vision
Human foveal vision is subserved initially by groups of spatial, temporal and orientational 'filters', the outputs of which are combined to define perceptual objects. Although a great deal is known about the filtering properties of individual cortical cells, relatively little is known about the nature of this 'linking' process. One recent approach has shown that the process can be thought of in terms of an association field whose strength is determined conjointly by the orientation and distance of the object. Here the authors describe a fundamental difference in this feature-linking process in central and peripheral parts of the visual field, which provides insight into the ways that foveal and peripheral visual perception differ. In the fovea, performance can be explained only by intercellular linking operations whereas in the periphery intracellular filtering will suffice. This difference represents a substantial economy in cortical neuronal processing of peripheral visual information and may allow a recent theory of intercellular binding to be tested.
R F Hess & S C Dakin
Absence of contour linking in peripheral vision (Letter to Nature)
Nature 390, 602 (1997)
Fear conditioning induces associative long-term potentiation in the amygdala
Long-term potentiation (LTP) is an experience-dependent form of neural plasticity believed to involve mechanisms that underlie memory formation. LTP has been studied most extensively in the hippocampus, but the relation between hippocampal LTP and memory has been difficult to establish. Here the authors explore the relation between LTP and memory in fear conditioning, an amygdala-dependent form of learning in which an innocuous conditioned stimulus (CS) elicits fear responses after being associatively paired with an aversive unconditioned stimulus (US). They have previously shown that LTP induction in pathways that transmit auditory CS information to the lateral nucleus of the amygdala (LA) increases auditory-evoked field potentials in this nucleus. Now they show that fear conditioning alters auditory CS-evoked responses in LA in the same way as LTP induction. The changes parallel the acquisition of CS-elicited fear behaviour, are enduring, and do not occur if the CS and US remain unpaired. LTP-like associative processes thus occur during fear conditioning, and these may underlie the long-term associative plasticity that constitutes memory of the conditioning experience.
M T Rogan, U V Stšubli & J E LeDoux
Fear conditioning induces associative long-term potentiation in the amygdala (Letter to Nature)
Nature 390, 604 (1997)
Fear conditioning induces a lasting potentiation of synaptic currents in vitro
The amygdala plays a critical role in the mediation of emotional responses, particularly fear, in both humans and animals. Fear conditioning, a conditioned learning paradigm, has served as a model for emotional learning in animals, and the neuroanatomical circuitry underlying the auditory fear-conditioning paradigm is well characterized. Synaptic transmission in the medial geniculate nucleus (MGN) to lateral nucleus of the amygdala (LA) pathway, a key segment of the auditory fear conditioning circuit, is mediated largely through N- methyl-D-aspartate (NMDA) and non-NMDA (such as alpha-amino-3-hydroxy-5-methyl-4- isoxazolepropionic acid (AMPA)) glutamate receptors; the potential for neural plasticity in this pathway is suggested by its capacity to support long-term potentiation (LTP). Here the authors report a long-lasting increase in the synaptic efficacy of the MGN--LA pathway attributable to fear-conditioning itself, rather than an electrically induced model of learning. Fear-conditioned animals show a presynaptic facilitation of AMPA-receptor-mediated transmission, directly measured in vitro with whole-cell recordings in lateral amygdala neurons. These findings represent one of the first in vitro measures of synaptic plasticity resulting from emotional learning by whole animals.
M G McKernan & P Shinnick-Gallagher
Fear conditioning induces a lasting potentiation of synaptic currents in vitro (Letter to Nature)
Nature 390, 607 (1997)
How opioids inhibit GABA-mediated neurotransmission
The midbrain region periaqueductal grey (PAG) is rich in opioid receptors and endogenous opioids and is a major target of analgesic action in the central nervous system. It has been proposed that the analgesic effect of opioids on the PAG works by suppressing the inhibitory influence of the neurotransmitter GABA (gamma-aminobutyric acid) on neurons that form part of a descending antinociceptive pathway. Opioids inhibit GABA-mediated (GABAergic) synaptic transmission in the PAG and other brain regions by reducing the probability of presynaptic neurotransmitter release, but the mechanisms involved remain uncertain. Here the authors report that opioid inhibition of GABAergic synaptic currents in the PAG is controlled by a presynaptic voltage-dependent potassium conductance. Opioid receptors of the type in GABAergic presynaptic terminals are specifically coupled to this potassium conductance by a pathway involving phospholipase A2, arachidonic acid and 12-lipoxygenase. Furthermore, opioid inhibition of GABAergic synaptic transmission is potentiated by inhibitors of the enzymes cyclooxygenase and 5-lipoxygenase, presumably because more arachidonic acid is available for conversion to 12-lipoxygenase products. These mechanisms account for the analgesic action of cyclooxygenase inhibitors in the PAG and their synergism with opioids.
C W Vaughan, S L Ingram, M A Connor & M J Christie
How opioids inhibit GABA-mediated neurotransmission
(Letter to Nature)

Nature 390, 611 (1997)
A Schwann cell mitogen accompanying regeneration of motor neurons
Motor neurons are the only adult mammalian neurons of the central nervous system to regenerate following injury. This ability is dependent on the environment of the peripheral nerve and an intrinsic capacity of motor neurons for regrowth. The authors report here the identification, using a technique known as messenger RNA differential display, of an extracellular signalling molecule, previously described as the pancreatic secreted protein Reg- 2, that is expressed solely in regenerating and developing rat motor and sensory neurons. Axon-stimulated Schwann cell proliferation is necessary for successful regeneration, and the authors show that Reg-2 is a potent Schwann cell mitogen in vitro. In vivo, Reg-2 protein is transported along regrowing axons and inhibition of Reg-2 signalling significantly rEtards the regeneration of Reg-2-containing axons. During development, Reg-2 production by motor and sensory neurons is regulated by contact with peripheral targets. Strong candidates for peripheral factors regulating Reg-2 production are cytokines of the LIF/CNTF family, because Reg-2 is not expressed in developing motor or sensory neurons of mice carrying a targeted disruption of the LIF receptor gene, a common component of the receptor complexes for all of the LIF/CNTF family.
F J Livesey, J A O'Brien, M Li, A G Smith, L J Murphy & S P Hunt
A Schwann cell mitogen accompanying regeneration of motor neurons (Letter to Nature)
Nature 390, 614 (1997)
Role of cytosolic phospholipase A2 in allergic response and parturition
Phospholipase A2 (PLA2) comprises a superfamily of enzymes that hydrolyse the ester bond of phospholipids at the sn-2 position. Among the members of this superfamily, cytosolic PLA2 has attracted attention because it preferentially hydrolyses arachidonoyl phospholipids and is activated by submicromolar concentrations of Ca2+ ions and by phosphorylation by mitogen-activated protein kinases (MAP kinases). Here the authors investigate the function of cytosolic PLA2 in vivo by using homologous recombination to generate mice deficient in this enzyme. These mice showed a marked decrease in their production of eicosanoids and platelet-activating factor in peritoneal macrophages. Their ovalbumin- induced anaphylactic responses were significantly reduced, as was their bronchial reactivity to methacholine. Female mutant mice failed to deliver offspring, but these could be rescued by administration of a progesterone-receptor antagonist to the mother at term. Considered together with previous findings, our results indicate that cytosolic PLA2 plays a non-redundant role in allergic responses and reproductive physiology.
N Uozumi, K Kume, T Nagase, N Nakatani, S Ishii, F Tashiro,
Y Komagata, K Maki, K Ikuta, Y Ouchi, J-i Miyazaki & T Shimizu

Role of cytosolic phospholipase A2 in allergic response and parturition (Letter to Nature)
Nature 390, 618 (1997)
Reduced fertility and postischaemic brain injury in mice deficient in cytosolic phospholipase A2
Phospholipase A2 (PLA2) enzymes are critical regulators of prostaglandin and leukotriene synthesis and can directly modify the composition of cellular membranes. PLA2 enzymes release fatty acids and lysophospholipids, including the precursor of platelet-activating factor, PAF, from phospholipids. Free fatty acids, eicosanoids, lysophospholipids and PAF are potent regulators of inflammation, reproduction and neurotoxicity. The physiological roles of the various forms of PLA2 are not well defined. The cytosolic form, cPL2, preferentially releases arachidonic acid from phospholipids and is regulated by changes in intracellular calcium concentration. The authors have now created 'knockout' (cPLA2-/-) mice that lack this enzyme, in order to evaluate its physiological importance. They find that cPLA2-/- mice develop normally, but that the females produce only small litters in which the pups are usually dead. Stimulated peritoneal macrophages from cPLA2-/- animals did not produce prostaglandin E2 or leukotriene B4 or C4. After transient middle cerebral artery occlusion, cPLA2-/- mice had smaller infarcts and developed less brain oedema and fewer neurological deficits. Thus cPLA2 is important for macrophage production of inflammatory mediators, fertility, and in the pathophysiology of neuronal death after transient focal cerebral ischaemia.
J V Bonventre, Z Huang, M R Taheri, E O'Leary, E Li, M A Moskowitz & A Sapirstein
Reduced fertility and postischaemic brain injury in mice deficient in cytosolic phospholipase A2 (Letter to Nature)
Nature 390, 622 (1997)
Miranda directs Prospero to a daughter cell during Drosophila asymmetric divisions
Asymmetric cell division is a general process used in many developmental contexts to create two differently fated cells from a single progenitor cell. Intrinsic mechanisms like the asymmetric transmission of cell-fate determinants during cell division, and extrinsic cell- interaction mechanisms, can mediate asymmetric divisions. During embryonic development of the Drosophila central nervous system, neural stem cells called neuroblasts divide asymmetrically to produce another multipotent neuroblast and a ganglion mother cell (GMC) of more restricted developmental potential. Intrinsic mechanisms promote asymmetric division of neuroblasts: for example, the transcription factor Prospero localizes to the basal cell cortex of mitotic neuroblasts and then segregates exclusively into the GMC, which buds off from the basal side of the neuroblast. In the GMC, Prospero translocates to the nucleus, where it establishes differential gene expression between sibling cells. Here the authors report the identification of a gene, miranda, which encodes a new protein that co-localizes with Prospero in mitotic neuroblasts, tethers Prospero to the basal cortex of mitotic neuroblasts, directing Prospero into the GMC, and releases Prospero from the cell cortex within GMCs. miranda thus creates intrinsic differences between sibling cells by mediating the asymmetric segregation of a transcription factor into only one daughter cell during neural stem-cell division.
H Ikeshima-Kataoka, J B Skeath, Y-i Nabeshima, C Q Doe
& F Matsuzaki

Miranda directs Prospero to a daughter cell during Drosophila asymmetric divisions (Letter to Nature)
Nature 390, 625 (1997)
Antiproliferative action of interferon-alpha requires components of T-cell-receptor signalling
Signal transduction through both cytokine and lymphocyte antigen receptors shares some common pathways by which they initiate cellular responses, such as activation of mitogen- activated protein kinase(s). However, other signalling components appear to be uniquely coupled to each receptor. For example, the interferon receptors transduce regulatory signals through the JAK/STAT pathway, resulting in an inhibition of growth and of antiviral effects, whereas this pathway apparently plays no role in T-cell-receptor (TCR)-dependent gene expression. Conversely, signal transduction through the TCR requires the tyrosine kinases Lck and ZAP-70 and the tyrosine phosphatase CD45. Here the authors show that, unexpectedly, transmission of growth-inhibitory signals by interferon-alpha (IFN-alpha) in T cells requires the expression and association of CD45, Lck and ZAP-70 with the IFN-alpha- receptor signalling complex.
E F Petricoin III, S Ito, B L Williams, S Audet, L F Stancato,
A Gamero, K Clouse, P Grimley, A Weiss, J Beeler, D S Finbloom,
E W Shores, R Abraham & A C Larner

Antiproliferative action of interferon-alpha requires components of T-cell-receptor signalling (Letter to Nature)
Nature 390, 629 (1997)
Cdc42 and Rac1 induce integrin-mediated cell motility and invasiveness through PI(3)K
Transformation of mammary epithelial cells into invasive carcinoma results in alterations in their integrin-mediated responses to the extracellular matrix, including a loss of normal epithelial polarization and differentiation, and a switch to a more motile, invasive phenotype. Changes in the actin cytoskeleton associated with this switch suggest that the small GTPases Cdc42 and Rac, which regulate actin organization, might modulate motility and invasion. However, the role of Cdc42 and Rac1 in epithelial cells, especially with respect to integrin- mediated events, has not been well characterized. Here the authors show that activation of Cdc42 and Rac1 disrupts the normal polarization of mammary epithelial cells in a collagenous matrix, and promotes motility and invasion. This motility does not require the activation of PAK, JNK, p70 S6 kinase, or Rho, but instead requires phosphatidylinositol-3- OH kinase (PI(3)K). Further, direct PI(3)K activation is sufficient to disrupt epithelial polarization and induce cell motility and invasion. PI(3)K inhibition also disrupts actin structures, suggesting that activation of PI(3)K by Cdc42 and Rac1 alters actin organization, leading to increased motility and invasiveness.
P J Keely, J K Westwick, I P Whitehead, C J Der & L V Parise
Cdc42 and Rac1 induce integrin-mediated cell motility and invasiveness through PI(3)K (Letter to Nature)
Nature 390, 632 (1997)
An extended microtubule-binding structure within the dynein motor domain
Flagellar dynein was discovered over 30 years ago as the first motor protein capable of generating force along microtubules. A cytoplasmic form of dynein has also been identified which is involved in mitosis and a wide range of other intracellular movements. Rapid progress has been made on understanding the mechanism of force production by kinesins and myosins. In contrast, progress in understanding the dyneins has been limited by their great size (relative molecular mass 1,000K--2,000K) and subunit complexity. The authors now report evidence that the entire carboxy-terminal two-thirds of the 532K force-producing heavy chain subunit is required for ATP-binding activity. They further identify a microtubule-binding domain, which, surprisingly, lies well downstream of the entire ATPase region and is predicted to form a hairpin-like stalk. Direct ultrastructural analysis of a recombinant fragment confirms this model, and suggests that the mechanism for dynein force production differs substantially from that of other motor proteins.
M A Gee, J E Heuser & R B Vallee
An extended microtubule-binding structure within the dynein motor domain (Letter to Nature)
Nature 390, 636 (1997)
Structure of the proteasome activator REG-alpha (PA28-alpha)
The specificity of the 20S proteasome, which degrades many intracellular proteins, is regulated by protein complexes that bind to one or both ends of the cylindrical proteasome structure. One of these regulatory complexes, the 11S regulator (known as REG or PA28), stimulates proteasome peptidase activity, and enhances the production of antigenic peptides for presentation by class I molecules of the major histocompatibility complex (MHC). The three REG subunits that have been identified, REG-alpha, REG-bEta and REG-gamma (also known as the Ki antigen), share extensive sequence similarity, apart from a highly variable internal segment of 17--34 residues which may confer subunit-specific properties. REG-alpha and REG-bEta preferentially form a heteromeric complex, although purified REG-alpha forms a heptamer in solution and has biochemical properties similar to the heteromeric REG- alpha/REG-bEta complex. The authors have now determined the crystal structure of human recombinant REG-alpha at 2.8 Å resolution. The heptameric barrel-shaped assembly contains a central channel that has an opening of 20 diameter at one end and another of 30 Ådiameter at the presumed proteasome-binding surface. The binding of REG probably causes conformational changes that open a pore in the proteasome alpha-subunits through which substrates and products can pass.
J R Knowlton, S C Johnston, F G Whitby, C Realini, Z Zhang,
M Rechsteiner & C P Hill

Structure of the proteasome activator REG-alpha (PA28-alpha) (Letter to Nature)
Nature 390, 639 (1997)
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