Disease relevance of Dll1

• The capacity of an adenovirus encoding the mature form of vascular endothelial growth factor (VEGF)-D, VEGF-D Delta N Delta C, to induce angiogenesis, lymphangiogenesis, or both was analyzed in 2 distinct in vivo models [1].
• The capacity of Ad-VEGF-D Delta N Delta C to induce endothelial cell proliferation, angiogenesis, and lymphangiogenesis demonstrates that its potential usefulness for the treatment of coronary artery disease, cerebral ischemia, peripheral vascular disease, restenosis, and tissue edema should be tested in preclinical models [1].
• SR increased the tachycardia that follows MI (change [Delta] in heart rate [HR] = 107 +/- 21 beats/min vs. 49 +/- 9 beats/min in control rats, p < 0.05) [2].
• Role of central mu, delta-1, and kappa-1 opioid receptors in opioid-induced muscle rigidity in the rat [3].
• Activation of spinal delta-1 or delta-2 opioid receptors reduces carrageenan-induced hyperalgesia in the rat [4].

Psychiatry related information on Dll1

• These include fragmentation of sleep, increased wake time, decrease in the length of sleep bouts, decrease in the amplitude of the diurnal rhythm of sleep, decrease in rapid eye movement sleep and a profound decrease in electroencephalogram Delta power (0.3-4 Hz) [5].
• Co-administered Delta 9-THC provided protection against the long-term increases in anxiety seen in the emergence test, but not the social interaction test, 6 weeks after MDMA treatment [6].
• Microinjection of the delta-1 opioid receptor agonist [D-Pen2,D-Pen5]enkephalin (DPDPE) or the delta-2 opioid receptor agonist [D-Ala2, Glu4]deltorphin (DELT) in the VMM increased response latency in the radiant heat tail-flick test with respective ED50 values (95% CL) of 0.66 (0.07-1.5) nmol and 0.1 (0.03-0.21) nmol [7].
• Significant increases in Delta sleep duration, with significant decreases in light sleep and wakefulness were observed during the repeated exposure to zolpidem [8].
• delta 9-tetrahydrocannabinol (THC)-induced alterations in limbic and neocortical function are associated with deficiencies in short-term memory and recall [9].

High impact information on Dll1

• Progesterone receptor and dopamine receptors are required in Delta 9-tetrahydrocannabinol modulation of sexual receptivity in female rats [10].
• The fact that activation of alphabetagamma-rENaC by DeltaP can be reproduced by the imposition of Deltapi suggests that water movement through the channel is also an important determinant of channel activity [11].
• In this model, a proangiogenic effect of Ad-VEGF-D Delta N Delta C was evident as early as 5 days after injection [1].
• We found that recombinant Bax (rBax, 10 and 100 ng/ml) induces a loss in mitochondrial membrane potential (Delta Psi m) [12].
• CPS-induced apoptosis involved intracellular free calcium (Ca2+) influx, phosphatidylserine exposure, mitochondrial permeability transmembrane pore (PTP) opening and mitochondrial transmembrane potential (Delta Psi m) dissipation leading to cytochrome c release, activation of caspase-9 and -3 and oligonucleosomal DNA fragmentation [13].

Chemical compound and disease context of Dll1

• Liver mitochondrial bioenergetics of Goto-Kakizaki (GK) rats (a model of non-insulin dependent diabetes mellitus) reveals a Delta Psi upon energization with succinate significantly increased relatively to control animals [14].
• Stimulation of cannabinoid receptors, the pharmacological target of Delta 9-tetrahydrocannabinol, is emerging as a promising therapy to alleviate levodopa-associated dyskinesias [15].
• delta 9-Tetrahydrocannabinol and anandamide enhance the ability of muscimol to induce catalepsy in the globus pallidus of rats [16].
• KC 12291 and R 56865 dose-dependently induced bradycardia (Delta heart rate obtained, -55.1+/-5.2 beat per min, P<0.05, and -71.9+/-8.5 bpm, P<0.05, respectively) [17].
• The effects of the selective delta-1 (delta(1)) opioid receptor agonist, DPDPE, and the selective delta(2) opioid receptor agonist, DSLET, have been studied on the ventricular fibrillation threshold (VFT) in rats with an experimental post-infarction cardiosclerosis (CS) [18].

Biological context of Dll1

• A reduction in mitochondrial transmembrane potential (Delta psi(m)) occurred considerably later than cytochrome c translocation [19].
• The anti-apoptotic protein Bcl-2 and the pancaspase inhibitor zVAD-fmk did not prevent cytochrome c release, but completely blocked the reduction in Delta psi(m), DNA fragmentation and apoptosis [19].
• Taken together these results suggest that the serum factor in conjunction with the immune cells may be participating in the efficient rejection of the tumor in syngeneic hosts and Delta psi(m) disruption but not cytochrome c release, is a critical and decisive event to trigger apoptotic cell death induced by the serum factor in AK-5 tumor cells [19].
• Endogenous activation of mu and delta-1 opioid receptors is required for long-term potentiation induction in the lateral perforant path: dependence on GABAergic inhibition [20].
• Bath application of the mu receptor agonist [D-Ala2, N-MePhe4, Gly5-ol]enkephalin (DAMGO) or the delta 1 receptor agonist [D-Pen2, D-Pen5]enkephalin (DPDPE) produced a long-linear, concentration-dependent reduction in the amplitude of the evoked EPSP/EPSC [21].

Anatomical context of Dll1

• Inhibitory actions of delta 1-, delta 2-, and mu-opioid receptor agonists on excitatory transmission in lamina II neurons of adult rat spinal cord [21].
• Possibly connected to the RNA editing mechanism, GluR-B was the only subunit whose RNA was concentrated in motor neuron cell nuclei in addition to the cytoplasm. delta-1 and -2 mRNAs were found at low levels throughout the gray matter [22].
• In ATP-energized mitochondria, ceramides do not alter Delta Psi, neither when cyto c is oxidized nor when it is reduced, ruling out a nonspecific disturbance by ceramides of mitochondrial membrane integrity [23].
• delta 4-3-Ketosteroid 5 beta-reductase was purified from male rat liver cytosol [24].
• Cultured hepatocytes did not express Delta-like, a specific marker for oval cells and hepatoblasts [25].

Associations of Dll1 with chemical compounds

• The antibody recognizes both delta 1 and delta 2 but not AMPA, kainate, NMDA, and mGluR1 alpha glutamate receptor subunits based on Western blot analysis of transfected HEK-293 cells [26].
• These abnormalities are associated with high basal ATP levels but a decreased glucose-induced ATP production (Delta of increment over baseline 0.7 +/- 0.5 or 0.5 +/- 0.3 pmol/islet in islets exposed to glucose or FFA vs. 12.0 +/- 0.6 in control islets, n = 3; P < 0.01) and, as a consequence, with an altered ATP/ADP ratio [27].
• It was previously found that the 85-kDa protein purified from rat brain using an inositol 1,4,5-trisphosphate (Ins(1,4,5)P3)-immobilized matrix was the delta 1 isoform of phosphatidylinositol-specific phospholipase C (PLC) [28].
• delta 4-3-Ketosteroid 5 beta-reductase was purified about 230-fold from 100,000 X g supernatant of rat liver homogenate using 7 alpha-hydroxy-4-cholesten-3-one as substrate throughout [29].
• In urethane anesthetized Sprague Dawley rats or C57BL/6 mice, functional magnetic resonance imaging was used to noninvasively measure the change in retinal oxygen tension (Delta PO(2)) during a carbogen-inhalation challenge [30].

Physical interactions of Dll1

• Recent data suggest that Notch receptors and their membrane-bound ligands Delta and Serrate are involved in both patterning and cell fate determination during odontogenesis [31].

Regulatory relationships of Dll1

• delta 1Tetrahydrocannabinol (THC) acutely suppresses tonic serum luteinizing hormone (LH) and prolactin levels in adult male rats [32].

Other interactions of Dll1

• Notch 1 and Delta were found to be expressed in the neural retina during the period of cell fate determination and differentiation [33].
• In line with these findings, all three tested COX inhibitors provoked significant and sustained decreases (Delta approximately -20%) in medullary blood flow (MBF), which were similar in magnitude and duration in control animals [34].
• Staining of the postsynaptic density and membrane of the granule cell-parallel fiber/cartwheel cell spins synapse was most prevalent with delta 1/2 and mGluR1 alpha antibodies [35].
• Only the highest concentration of IGF-1 elicited an inhibition on Delta FFI in sucrose myocytes [36].
• The mitochondrial death pathway was suggested to be involved in BITC-induced apoptosis because the treatment of cells with BITC-induced caspase-9-dependent apoptosis and mitochondrial transmembrane potential (Delta Psi m) alteration [37].

Analytical, diagnostic and therapeutic context of Dll1

• The 3D structures of the full-length and a C-terminal deletion (Delta C) mutant of Shaker were determined by electron microscopy and single-particle analysis [38].
• This study examined the electrophysiological consequences of selective activation of delta 1-, delta 2-, or mu-opioid receptors using whole-cell recordings made from visually identified lamina II neurons in thin transverse slices of young adult rat lumbar spinal cord [21].
• The aortic PCR product was cloned and sequenced and found to represent two novel subunit sequences, designated delta 2 and delta 3 to distinguish them from the previously described delta sequence (now called delta 1) from brain. delta 2 was identical to the predicted delta 1 sequence except for a deletion of 102 base pairs (bp) [39].
• Real-time whole cell fluorescence video microscopy was utilized to analyze mitochondrial inner membrane potential (Delta Psi(m)), which drives ATP synthesis, in cultured adult sensory neurons [40].
• In each instance, receptor affinity was diminished by 1,2 unsaturation, but this effect was offset by the greater bioavailability of the delta 1 derivatives on oral administration [41].

References