Disease relevance of Pttg1ip

• In this study we investigated the gene expression of TGF-beta 1 mRNA and EGF mRNA and other parameters of the pancreas including DNA synthesis, blood flow (PBF), tissue protein content and plasma amylase during the induction of acute pancreatitis [1].

High impact information on Pttg1ip

• On sucrose gradients, urea-denatured pOTC sedimented to the bottom, whereas PBF sedimented with an S20,w value of 5.5S [2].
• The purified PBF markedly stimulated the import of purified or in vitro synthesized pOTC into the mitochondria [2].
• Additional evidence indicates that HNF-3beta and PBF cooperatively interact with enhancer 1 [3].
• When the purified PBF was readded to the depleted lysate, pOTC sedimented as a complex of about 7 S. In contrast to most mitochondrial proteins, rat 3-oxoacyl-CoA thiolase is synthesized with no cleavable presequence and an NH2-terminal portion of the mature protein functions as a mitochondrial import signal [4].
• L-NAME 3.7 nmol x kg(-1) x min(-1) improved PBF autoregulation by lowering PBF to the range of 100 to 140 mm Hg of perfusion pressure, and this effect was attenuated or abolished by valsartan in innervated and denervated kidneys, respectively [5].

Biological context of Pttg1ip

• Therefore, a higher dose of L-NAME induces a renal cortical vasoconstriction through potentiation of the renin-angiotensin system, whereas the fall of PBF seen after L-NAME 37 nmol x kg(-1) x min(-1) seems to be caused primarily by NO suppression [5].
• In anaesthetised Wistar rats, total renal blood flow (RBF) was measured, as was cortical (CBF) and papillary (PBF) blood flow, using the laser-Doppler technique, in responses to Ang II (30 ng kg(-1) min(-1)) alone and after ACE inhibition (enalapril) or bradykinin/prostaglandin synthesis inhibition (ketoprofen, aprotinin) [6].

Anatomical context of Pttg1ip

• To clarify the role of nitric oxide (NO) in the pancreas, blood flow in the rat pancreas (pancreatic blood flow: PBF) was investigated by the hydrogen clearance technique using a specific NO synthase inhibitor, N omega-nitro-L-arginine (L-NNA) [7].
• With this method, PBF is calculated indirectly from the sums of the blood flow of the splanchnic organs that drain into the portal vein [8].

Associations of Pttg1ip with chemical compounds

• The caerulein-induced increase in PBF was not affected significantly by atropine sulfate (100 micrograms/kg), nor by phenoxybenzamine (5 mg/kg) plus propranolol (50 micrograms/kg) [7].
• When Ang II was infused PBF and MAP increased markedly [6].
• (iii) Enalapril treatment left PBF unchanged but decreased MAP and increased RBF and CBF [6].
• (ii) Treatment with aprotinin and ketoprofen left MAP, RBF and CBF unchanged but decreased PBF [6].
• (iv) L-NAME reduced PBF independently of losartan treatment [6].

Analytical, diagnostic and therapeutic context of Pttg1ip

• The purified PBF migrated as a single polypeptide of 50,000 daltons on SDS-PAGE [2].
• A protein factor that binds to pOTC but not to mature OTC and was named presequence binding factor or PBF, was purified 91,000-fold from the lysate by affinity chromatography using pOTC-bound Sepharose, DEAE-5PW HPLC and sucrose gradient centrifugation [2].
• Cortical (CBF) and papillary (PBF) blood flow were measured by laser-Doppler flowmetry [5].

References