Bringing the State Back In

Book reviewed in this article:
Culture and Society in New Order Indonesia . Virginia Matheson Hooker , ed. Kuala Lumpur: Oxford University Press, 1993. 302 pp. Dissociated Identities: Ethnicity, Religion, and Class in an Indonesian Society . Rita Smith Kipp. Ann Arbor: University of Michigan Press, 1993. 320 pp.     

HMG-D is an architecture-specific protein that preferentially binds to DNA containing the dinucleotide TG.

The high mobility group (HMG) protein HMG-D from Drosophila melanogaster is a highly abundant chromosomal protein that is closely related to the vertebrate HMG domain proteins HMG1 and HMG2. In general, chromosomal HMG domain proteins lack sequence specificity. However, using both NMR spectroscopy and standard biochemical techniques we show that binding of HMG-D to a single DNA site is sequence selective. The preferred duplex DNA binding site comprises at least 5 bp and contains the deformable dinucleotide TG embedded in A/T-rich sequences. The TG motif constitutes a common core element in the binding sites of the well-characterized sequence-specific HMG domain proteins. We show that a conserved aromatic residue in helix 1 of the HMG domain may be involved in recognition of this core sequence. In common with other HMG domain proteins HMG-D binds preferentially to DNA sites that are stably bent and underwound, therefore HMG-D can be considered an architecture-specific protein. Finally, we show that HMG-D bends DNA and may confer a superhelical DNA conformation at a natural DNA binding site in the Drosophila fushi tarazu scaffold-associated region.     

Floxed allele for conditional inactivation of the GABAB(1) gene

GABA(B) receptors are the G-protein-coupled receptors for the neurotransmitter GABA. GABA(B) receptors are broadly expressed in the nervous system. Their complete absence in mice causes premature lethality or--when mice are viable--epilepsy, impaired memory, hyperalgesia, hypothermia, and hyperactivity. A spatially and temporally restricted loss of GABA(B) function would allow addressing how the absence of GABA(B) receptors leads to these diverse phenotypes. To permit a conditional gene inactivation, we flanked critical exons of the GABA(B(1)) gene with lox511 sites. GABA(B(1)) (lox511/lox511) mice exhibit normal levels of GABA(B(1)) protein, are fertile, and do not display any behavioral phenotype. We crossed GABA(B(1)) (lox511/lox511) with Cre-deleter mice to produce mice with an unrestricted GABA(B) receptor elimination. These GABA(B(1)) (-/-) mice no longer synthesize GABA(B(1)) protein and exhibit the expected behavioral abnormalities. The conditional GABA(B(1)) allele described here is therefore suitable for generating mice with a site- and time-specific loss of GABA(B) function.     

Serine 727 phosphorylation and activation of cytosolic phospholipase A2 by MNK1-related protein kinases

We have previously reported that in thrombin-stimulated human platelets, cytosolic phospholipase A(2) (cPLA2) is phosphorylated on Ser-505 by p38 protein kinase and on Ser-727 by an unknown kinase. Pharmacological inhibition of p38 leads to inhibition of cPLA2 phosphorylation at both Ser-505 and Ser-727 suggesting that the kinase responsible for phosphorylation on Ser-727 is activated in a p38-dependent pathway. By using Chinese hamster ovary, HeLa, and HEK293 cells stably transfected with wild type and phosphorylation site mutant forms of cPLA2, we show that phosphorylation of cPLA2 at both Ser-505 and Ser-727 and elevation of Ca(2+) leads to its activation in agonist-stimulated cells. The p38-activated protein kinases MNK1, MSK1, and PRAK1 phosphorylate cPLA2 in vitro uniquely on Ser-727 as shown by mass spectrometry. Furthermore, MNK1 and PRAK1, but not MSK1, is present in platelets and undergo modest activation in response to thrombin. Expression of a dominant negative form of MNK1 in HEK293 cells leads to significant inhibition of cPLA2-mediated arachidonate release. The results suggest that MNK1 or a closely related kinase is responsible for in vivo phosphorylation of cPLA2 on Ser-727.     

Global Violence and Indonesian Muslim Politics

The attacks of September 11, 2001, in the United States and the U.S.-led campaign in Afghanistan provoked fierce threats of violence in Indonesia, the world's largest majority-Muslim country. Western journalists portrayed these reactions as among the most destabilizing in the Muslim world. Less widely reported, however, was the intensification of a struggle between Muslim proponents of democracy and neof undamentalist conservatives, sparked by the same incidents. This article explores the varied reactions of Muslims to the violence of September 11 and its aftermath in light of this contest between rival Muslim groupings. It examines their competing visions of Islam and nation, as well as their supporting alliances in state and society. The example highlights the pluralism of Muslim politics and the special challenges of democratic transitions. Emphasizing the plurality and permeability of civilizations, the example also suggests that there is no "clash of civilizations" between Islam and the West but, rather, a more open process of globalization, localization, and exchange. [Keywords: Islam, Indonesia, violence, democratization, civilization]     

From Cosmogony to Exorcism in a Javanese Genesis.

From Cosmogony to Exorcism in. Javanese Genesis. Stephen C. Headley. New York: Oxford University Press, 2000. 250 pp.     

VEGF modulates erythropoiesis through regulation of adult hepatic erythropoietin synthesis

Vascular endothelial growth factor (VEGF) exerts crucial functions during pathological angiogenesis and normal physiology. We observed increased hematocrit (60-75%) after high-grade inhibition of VEGF by diverse methods, including adenoviral expression of soluble VEGF receptor (VEGFR) ectodomains, recombinant VEGF Trap protein and the VEGFR2-selective antibody DC101. Increased production of red blood cells (erythrocytosis) occurred in both mouse and primate models, and was associated with near-complete neutralization of VEGF corneal micropocket angiogenesis. High-grade inhibition of VEGF induced hepatic synthesis of erythropoietin (Epo, encoded by Epo) >40-fold through a HIF-1alpha-independent mechanism, in parallel with suppression of renal Epo mRNA. Studies using hepatocyte-specific deletion of the Vegfa gene and hepatocyte-endothelial cell cocultures indicated that blockade of VEGF induced hepatic Epo by interfering with homeostatic VEGFR2-dependent paracrine signaling involving interactions between hepatocytes and endothelial cells. These data indicate that VEGF is a previously unsuspected negative regulator of hepatic Epo synthesis and erythropoiesis and suggest that levels of Epo and erythrocytosis could represent noninvasive surrogate markers for stringent blockade of VEGF in vivo.     

Infrared optical immunosensor: application to the measurement of the herbicide atrazine

A new approach to optically transduce antigen-antibody association, needing no label, is described herein, taking advantage of the ability of reflection-absorption infrared (IR) spectroscopy to analyze organic thin films at the surface of reflective materials with high sensitivity. As a proof-of-principle, this new technique was applied to the immunodetection of the herbicide atrazine. Gold-coated chips were covered with a capture layer consisting of a protein derivative of the herbicide atrazine covalently bound to a self-assembled monolayer containing a carboxy-terminated thiolate. Successive binding of anti-atrazine antibody and secondary anti-rabbit immunoglobulin G antibody resulted in a change of the IR absorption properties of the organic film at the sensor surface. The two prominent amide I and II bands observed on the surface IR spectra were taken for semiquantitative analysis of the adsorbed protein amount. The presence of increasing amounts of atrazine resulted in the progressive inhibition of antibodies binding to the sensors, yielding a relative lower increase of the IR signals. The deduced standard curves displayed a sigmoidal shape typical of competitive inhibition assays. The test midpoint (IC(50)) and the limit of detection (IC(80)) were found to be in the nanomolar range and very close to those measured by an in-house enzyme-linked immunosorbent assay using the same antibody and the same antigen competitor.