Disease relevance of ATP6AP1

• Moreover, a chronic myelogenous leukemia patient who experienced a complete remission after CD4(+) donor lymphocyte infusions also developed high-titer antibodies to ATP6S1 [1].
• Three additional vaccinated melanoma patients and three metastatic non-small cell lung carcinoma patients vaccinated with autologous GM-CSF-secreting tumor cells similarly showed a correlation between humoral responses to ATP6S1 and tumor destruction [1].
• A fraction of DNA from the human fetal lung fibroblast line IMR-90, 30-fold enriched for ribosomal DNA, was cloned in the lambda phage vector Charon 16A [2].
• Streptococcus pneumoniae type 16A, a hitherto undescribed pneumococcal type [3].
• Human placental DNA, enriched for ribosomal sequences, was cloned in the phage vector lambda Charon 16A [4].

Psychiatry related information on ATP6AP1

• An extended region of the greater mustached bat's cochlea, the sparsely innervated (SI) zone, is located just basally to the frequency place of the dominant 61-kHz component of the echolocation signal (CF2) [5].

High impact information on ATP6AP1

• A chimeric promoter containing six copies of the -181 to -171 region of Rab 16A fused to a minimal promoter conferred ABA-responsive expression on the reporter gene [6].
• Overexpression of XAP3 enhanced X transactivation activity [7].
• One of the activation domains of X (amino acids 90-122) is required for binding to XAP3, while the NH2-terminal part of XAP3 is necessary for binding to X [7].
• Both X and XAP3 bound specifically to the eta PKC isoenzyme synthesized in rabbit reticulocyte lysates [7].
• Hence, the cDNA encoding the protein Ac45 was cloned from a bovine adrenal medulla library [8].

Chemical compound and disease context of ATP6AP1

• Carbon dioxide absorbents, such as soda lime and Baralyme brand absorbent, convert sevoflurane to CF2 = C(CF3)OCH2F, a vinyl ether called "Compound A," whose toxicity raises concerns regarding the safety of sevoflurane in rebreathing circuits [9].
• Forty-four patients affected by nasal polyps were admitted to the Department of Otolaryngology, Lublin University School of Medicine, Lublin, Poland, and screened for the most-commonly identified CFTR mutations [DeltaF508, G542X, N1303 K, 1717-1 (G to A), W1282X, G551D, R553X and DeltaI507] by applying the INNO-LIPA CF2 test strips [10].

Biological context of ATP6AP1

• Furthermore, the overall degree of amino acid sequence identity between the mammalian and invertebrate Ac45 proteins is very low (<18%), except for a surprisingly highly conserved putative targeting motif in the carboxy-terminal region [11].
• Primer extension analysis revealed that the mouse Ac45 gene contains two major transcription initiation sites [11].
• The 26-residue cytoplasmic tail of Ac45 was intrinsically capable of mediating endocytosis of the cell surface protein Tac, indicating that the tail contains an autonomous internalization signal [12].
• Southern hybridization, PCR amplification, and DNA sequence analyses were performed on the toxin A (tcdA) and toxin B (tcdB) genes of type CF2 isolate 5340 [13].
• Type CF2 5340 tcdA exhibited a 1,821-bp truncation, due to three deletions in the 3' end of the gene, and a point mutation in the 5' end of the gene, resulting in a premature stop codon at tcdA position 139 [13].

Anatomical context of ATP6AP1

• We conclude that the regionally conserved Xenopus Ac45 protein is synthesized as an N-glycosylated approximately 60-kDa precursor that is intracellularly cleaved to an approximately 40-kDa product and speculate that it may assist in the V-ATPase-mediated acidification of neuroendocrine secretory granules [14].
• Experiments with a specific antibody against Ac45 demonstrated that it is copurifying with the V-ATPase from chromaffin granules [8].
• Steady state immunolabeling showed that Ac45 is located on the plasma membrane and in a vacuolar compartment in the juxtanuclear region [12].
• Ac45 is a type I transmembrane protein associated with vacuolar H+-ATPase, a proton pump mediating the acidification of multiple intracellular organelles [12].
• RESULTS: Significant enhancement of fluorescence for 16AP and NBD C(6)-HPC was evident in solutions incubated with whole tears and purified TL but not with tears depleted of TL for fixed and unfixed corneas [15].

Associations of ATP6AP1 with chemical compounds

• 1. Replacement of each amino acid on either loop by single tryptophan mutation does not disrupt the pH-dependent binding affinity to 16AP [16].
• In the transition from pH 7.5 to pH 5.5, the ligand affinity for 16-(9-anthroyloxy)palmitic acid (16AP) and 8-anilino-1-naphthalenesulfonic acid is reduced [16].
• RESULTS: Two degradation products, CF2 = C(CF3)-O-CH2F (compound A) and CH3OCF2CH(CF3)OCH2F (compound B), were detected [17].
• RESULTS: Among the breakdown products of sevoflurane, two products, CF2 = C(CF3)-O-CH2F (compound A) and CH3OCF2CH(CF3)OCH2F (compound B), were detected [18].
• BACKGROUND: An olefin called compound A (CF2 = C(CF3)OCH2F) results from the action of soda lime or Baralyme on sevoflurane [19].

Analytical, diagnostic and therapeutic context of ATP6AP1

• Western blot analysis showed that immunoreactive Ac45 represents a approximately 40-kDa product that is expressed predominantly in neuroendocrine tissues; deglycosylation resulted in a approximately 27-kDa immunoreactive Ac45 product which is smaller than predicted for the intact protein [14].
• REA type CF2 is a toxin variant strain of C. difficile that retains the ability to cause disease in humans but is not detected in clinical immunoassays for toxin A [13].
• This strain, identified by restriction endonuclease analysis (REA) as type CF2, was not detected by an immunoassay for C. difficile toxin A. Culture supernatants of CF2 failed to elicit significant enterotoxic activity in the rabbit ileal loop assay but did produce atypical cytopathic effects in cell culture assay [13].
• Bedside-inoculated 16A media is superior to the routine method for the recovery of microorganisms causing peritonitis in CAPD patients [20].
• Since targeted prolong release was observed in formulation CF2 and CF5, these formulations were further subjected to in vivo drug release study using rabbits as an animal model [21].

References