Disease relevance of Slc33a1

• At day 7, AT1(-/-) showed marked proteinuria to a similar extent to that of wild-type mice (WT) [1].
• Using the recently developed ELISPOT cloning methodology, we obtained cDNA clone S35 coding for the Ag epitope recognized by a murine sarcoma Meth A-specific CTL clone AT-1 [2].
• Many lines of evidence have suggested that angiotensin II (AngII) plays an important role in the development of cardiac hypertrophy through AngII type 1 receptor (AT1) [3].
• CONCLUSIONS: AT1 receptors play an important role in the development of fibrosis [4].
• Pharmacological blockade of AT1 receptors appears to be a promising approach to treat liver fibrosis [4].

High impact information on Slc33a1

• AT-1 precipitated a p60-65 protein from [35S]methionine-labeled activated B cells, similar to that from activated T cells [5].
• We have derived a cardiac muscle cell line, designated HL-1, from the AT-1 mouse atrial cardiomyocyte tumor lineage [6].
• Identification of a T-type Ca(2+) channel isoform in murine atrial myocytes (AT-1 cells) [7].
• The cloned T-type channels and AT-1 T-type current share similar kinetics of macroscopic inactivation and deactivation [7].
• These results suggest that AT1-mediated Ang II signaling is not essential for the development of neointimal formation, although it may modify it [8].

Chemical compound and disease context of Slc33a1

• METHODS: Therefore, linomide analogs were initially screened to determine their in vivo potency to inhibit growth of the Dunning R-3327 AT-1 rat prostate cancer model in rats and their potency to inhibit angiogenesis in a Matrigel assay in mice [9].

Biological context of Slc33a1

• Assignment1 of a putative acetyl-CoA transporter gene (Acatn) to mouse chromosome band 3E1-E3 by in situ hybridization [10].
• Atrial tumor myocytes derived from transgenic mice (AT-1 cells) maintain a well-differentiated cardiac biochemical and histological phenotype [11].
• Accordingly, the AT-1 cell system should provide a uniquely useful model to identify the intracellular targets for PKCepsilon and investigate their function in the regulation of intracellular calcium homeostasis and the induction of the growth response in cardiac myocytes [12].
• The major outward current in AT-1 cells is a delayed rectifier that displays prominent inward rectification, activates rapidly (eg, 182 +/- 27 milliseconds [mean +/- SEM] at + 20 mV, n = 12), exhibits biexponential deactivation kinetics, and is extremely sensitive to the methanesulfonanilide dofetilide (IC50, 12 nmol/L) [11].
• In this study, we identified the major depolarization-activated outward currents in AT-1 cells; also, the presence of mRNAs that encode outwardly conducting ion channels was determined by cloning from an AT-1 cDNA library or by Northern hybridization [11].

Anatomical context of Slc33a1

• K+ currents and K+ channel mRNA in cultured atrial cardiac myocytes (AT-1 cells) [11].
• Reverse transcriptase-polymerase chain reaction analysis revealed that AT1 mRNA was not detectable in both uninjured and injured carotid arteries of KO mice, whereas the AT1 gene was expressed in uninjured carotid arteries of wild-type (WT) mice [8].
• AT1(-/-) had a significantly higher ET-1 expression in tubular epithelial cells than WT [1].
• We have used sarcoplasmic reticulum (SR) vesicles isolated from AT-1 cardiomyocytes to examine the mechanism of phospholamban (PLB) inhibition of the Ca2+ pump of cardiac SR [13].
• The AT1 subline was found to be restricted to the expression of a single light chain type (lambda) indicating a possible B cell lineage-committed precursor as the target for viral transformation [14].

Associations of Slc33a1 with chemical compounds

• The acetyl-CoA transporter gene (Acatn) encodes a hydrophobic, multitransmembrane protein that is involved in the process of O-acetylation of sialic acid residues on gangliosides [15].
• IKr in AT-1 cells displayed slow inactivation: dofetilide-sensitive deactivating tails were greater after 1-second than after 5-second pulses [11].
• Moreover, treatment with the selective AT1 antagonist CV-11974 before injury significantly decreased the formation of neointima in only WT mice, whereas treatment with the selective AT2 antagonist PD-123319 before injury had no effects in both animal groups [8].
• However, the interstitial infiltration persisted in AT1(-/-) when treated with quinapril [1].
• These results suggest that mechanical stretch could evoke hypertrophic responses in cardiac myocytes that lack the AT1 signaling pathway possibly through tyrosine kinase activation [3].

Analytical, diagnostic and therapeutic context of Slc33a1

• Cultured AT-1 cells expressed AE2, cAE3, and bAE3 polypeptides, which were detected by immunoblot and immunocytochemistry [16].
• In addition, the feasibility of culturing AT-1 cells provides us with a system where electrophysiologic experiments on IKr currents could be combined with biochemical or molecular biological studies requiring significant periods of incubation in a cell culture system [17].
• In the group repeatedly treated with losartan, ex vivo autoradiography depicted the marked decrease in angiotensin II-binding capacity to the sites containing exclusively AT1 receptors within the blood-brain barrier [18].
• This constriction was completely abolished by an AT-1 antagonist, CV-11974 [19].

References