Anti-RHAG polyclonal antibody

Arylation with [Ag(C6F5)] or (NBu(4))[Ag(C6F5)(2)] of several rhodium or iridium substrates leads to new anionic complexes of type [M(C6F5)Cl(L(2))](-) (M = Rh, L(2) = (CO)2; M = Ir, L(2) = cod) or [M(C6F5)(2)(L(2))](-) (M = Rh, L(2) = (CP)(2), cod, {P(OPh)(3)}(2); M = Ir, L(2) = cod) which have been isolated as benzyltriphenylphosphonium or tetrabutylammonium salts. The reactivity of some of these complexes have been explored. Addition of neutral ligands to [Rh(C6F5)Cl(CO)(2)](-) gives neutral rhodium(I) complexes [Rh(C6F5)(PPh(3))(CO)(2)] and [Rh(C6F5)(CO)L] (L = 2,2'-bipyridine (bipy) or 1,10-phenanthroline (phen)); with bis(diphenylphosphino)methane (dppm), the A-frame compound [Rh-2(C6F5)(2)(mu-CO)mu-dppm)(2)] is prepared. Reactions of methyl iodide, [Tl(C6F5)(2)Cl], and [Ag(PPh(3))](+) with the rhodium(I) complexes are described. The new compounds I;ave been characterized by elemental analyses, MS, NMR, and conductivity and the heterobimetallic complex [{P(OPh)(3))(2)(C6F5)(2)RhAg(PPh(3))] has also been characterized by a single-crystal X-ray diffraction study. The crystals are triclinic (space group P (1) over bar) having a unit cell of dimensions a = 11.984(2) Angstrom, b = 12.752(2) Angstrom, c = 22.183(5) Angstrom, alpha = 101.07(1)degrees, beta = 104.14(1)degrees, gamma = 103.06(1)degrees, V = 3090.7(10) Angstrom 3, and Z = 2. The structure was solved by Patterson methods and refined by full-matrix least squares to R = 0.064, R(w) = 0.051 for 5802 observed reflections (F greater than or equal to 2 sigma(F)). The rhodium atom is in a square-pyramidal environment, with two C6F5 (cis) and two P(OPh)(3) ligands in the square plane and a Ag(PPh(3)) moiety in the apical position. The complex contains a Rh-Ag bond [2.635(1) Angstrom] unsupported by covalent bridges.

Fish early life stages have been shown to react sensitive to simulated ocean acidification. In particular, acid-base disturbances elicited by altered seawater carbonate chemistry have been shown to induce pathologies in larval fish. However, the mechanisms underlying these disturbances are largely unknown. We used gene expression profiling of genes involved in acid-base regulation and metabolism to investigate the effects of seawater hypercapnia on developing Japanese ricefish (medaka; Oryzias latipes). Our results demonstrate that embryos respond with delayed development during the time window of 2-5 dpf when exposed to a seawater pCO(2) of 0.12 and 0.42 kPa. This developmental delay is associated with strong down-regulation of genes from major metabolic pathways including glycolysis (G6PDH), Krebs cycle (CS) and the electron transport chain (CytC). In a second step we identified acid-base relevant genes in different ontogenetic stages (embryos, hatchlings and adults) and tissues (gill and intestine) that are up regulated in response to hypercapnia, including NHE3, NBCa, NBCb, AE1a, AEI b, ATP1a1a.1, A7P1a1b, ATP1b1a, Rhag, Rhbg and Rhcg. Interestingly, NHE3 and Rhcg expressions were increased in response to environmental hypercapnia in all ontogenetic stages and tissues tested, indicating the central role of these proteins in acid-base regulation. Furthermore, the increased expression of genes from amino acid metabolism pathways (ALT1, ALT2, AST1a, AST1b, AST2 and GLUD) suggests that energetic demands of hatchlings are fueled by the breakdown of amino acids. The present study provides a first detailed gene expression analysis throughout the ontogeny of a euryhaline teleost in response to seawater hypercapnia, indicating highest sensitivity in early embryonic stages, when functional ion regulatory epithelia are not yet developed. (C) 2013 Elsevier Inc. All rights reserved.