Disease relevance of ANKS1B

• From March 1993 to October 1993, 20 consecutive, newly diagnosed acute promyelocytic leukemia (APL) patients from 13 Italian institutions entered in a pilot study named AIDA, combining all-trans retinoic acid (ATRA) with idarubicin (IDA) [1].
• A modified AIDA protocol with anthracycline-based consolidation results in high antileukemic efficacy and reduced toxicity in newly diagnosed PML/RARalpha-positive acute promyelocytic leukemia. PETHEMA group [2].
• Invasion activity of a Mycobacterium tuberculosis peptide presented by the Escherichia coli AIDA autotransporter [3].
• Overall, patients were managed out of the hospital for 66% of the period of post-consolidation neutropenia (77%, 48% and 50% of the post-consolidation neutropenia period in patients treated with AIDA, AML10 and AML13 protocols, respectively) [4].
• Insertional gene disruption of sre prevented a lysogen from entering the lytic cycle, implying that Sre protein is a site-specific recombinase needed for excision of the R4 prophage genome (M. Matsuura, T. Noguchi, T. Aida, M. Asayama, H. Takahashi, and M. Shirai, J. Gen. Appl. Microbiol. 41:53-61, 1995) [5].

Psychiatry related information on ANKS1B

• The objective of the AIDA project (Artificial Intelligent Dental Agents, http://aida.uni-hd.de) is the analysis of dental decision-making, the design of a computer-based decision support system, as well as the testing of the decision structure in interactions with dental experts, practicing dentists, and patients [6].

High impact information on ANKS1B

• Furthermore, myosin X and the microtubule plus-end-tracking protein EB1 are shown to play a role in this mechanism through remodeling of actin cytoskeleton and stabilization of astral microtubules, respectively [7].
• Integrin-mediated adhesion orients the spindle parallel to the substratum in an EB1- and myosin X-dependent manner [7].
• A recently developed autocorrelation statistic summarizing molecular similarity at all sites (AIDA; autocorrelation index for DNA analysis) confirms the presence of a clinical pattern; differences between random pairs of haplotypes tend to increase with their geographical distance [8].
• The results of the Italian pediatric experience with the multicentric Gruppo Italiano per le Malattie Ematologiche dell'Adulto (GIMEMA)-Italian Pediatric Hematology and Oncology Group (AIEOP) "AIDA" (ATRA and idarubicin) trial are presented [9].
• Thirty-one APL-st and 641 de novo APL patients received homogeneous APL therapy according to the all-trans retinoic acid (ATRA) and idarubicin regimen (the AIDA regimen) [10].

Chemical compound and disease context of ANKS1B

• The Spanish PETHEMA group designed a protocol for newly diagnosed PML/RARalpha-positive acute promyelocytic leukemia (APL) in which induction and consolidation followed the original AIDA regimen, except for the omission of cytarabine and etoposide from consolidation [2].
• The Escherichia coli AIDA autotransporter adhesin recognizes an integral membrane glycoprotein as receptor [11].
• AIDA is a prototype computer system that incorporates a model of glucose-insulin interaction in type I diabetes mellitus alongside a knowledge-based system to make glycaemic predictions and to generate insulin dosage adjustment advice [12].

Biological context of ANKS1B

• Our data demonstrated that the interaction between the two molecules is regulated by alternative splicing of the AIDA-1 proteins [13].
• The genes involved in diffuse adhesion to HEp-2 cells were located on conjugative R plasmids in strains that did not hybridize with the DA or AIDA DNA probes [14].
• Novel roles for the AIDA adhesin from diarrheagenic Escherichia coli: cell aggregation and biofilm formation [15].
• AIDA treatment for high-risk acute promyelocytic leukemia in a pregnant woman at 21 weeks of gestation [16].
• The IC50 values calculated were: 8.7 x 10(-5), 4.3 x 10(-6) and 6.3 x 10(-7) M for AIDA, LY 367385 and MPEP, respectively [17].

Anatomical context of ANKS1B

• Prospective RT-PCR analyses were performed since 1993 at diagnosis and at preestablished time intervals during follow-up in bone marrow (BM) samples of 163 patients with PML/RARalpha+ APL enrolled in the multicenter Gruppo Italiano Malattie Ematologiche Maligne dell' Adulto (GIMEMA) trial AIDA (All-trans retinoic acid plus Idarubicin) [18].
• The EB-1 human cell line contains wild type p53 protein which fails to express the PAb421 epitope and is highly active both in biological assays and in DNA binding assays [19].
• METHODS: To increase the outflow of aqueous humor, ten microperforations of the trabecular meshwork were performed by an endoscope-guided photoablative laser probe (Excimer laser, AIDA, TUI-Laser, Munich; pulse energy: 1.2 mJ at fiber tip, pulse duration: 60 ns, repetition rate: 20 Hz) [20].
• In gerbils subjected to global ischemia, intracerebroventricular administration of AIDA (100 nmol two times) or CBPG (300 nmol, two times) afforded consistent protection against CA1 pyramidal cell death, whereas MPEP (10 pmol i.c.v two times and 10 mg/kg i.p two times) failed to reduce postischemic hippocampal damage [21].

Associations of ANKS1B with chemical compounds

• ATRA 45 mg/sqm/day was given to all patients, and in 11 was associated with idarubicin (AIDA protocol); in two patients ATRA was associated with mitoxantrone + ara-C, while the remaining three patients received ATRA alone [22].
• Similarly, AIDA (1 mM; n = 7) reversed the capsaicin-induced sensitization and also blocked the potentiation by S-DHPG (n = 5) [23].
• In normal awake conditions, the spontaneous firing rates of neurons in the pallidal complex were increased by DHPG, a selective agonist of group I mGluRs, whereas they were decreased by AIDA, a selective antagonist of group I mGluRs, or LY367385, a selective antagonist of mGluR1 [24].
• These include the use of simulated blood glucose data from the AIDA program for preliminary computerlab-based testing of other decision support prototypes [25].
• Hemoglobins Aida (alpha 64 Asp leads to Asn) and D-Los Angeles (beta 121 Glu leads to Gln) in an Asian-Indian family [26].

Other interactions of ANKS1B

• A novel EB-1/AIDA-1 isoform, AIDA-1c, interacts with the Cajal body protein coilin [27].
• siRNA-mediated inhibition of E2A-PBX1 reduces EB-1 and Wnt16b expression in 697 pre-B leukemia cells [28].

Analytical, diagnostic and therapeutic context of ANKS1B

• All patients had achieved first molecular remission after the AIDA protocol (all-trans retinoic acid [ATRA] + idarubicin) and were being prospectively monitored by reverse transcriptase-polymerase chain reaction (RT-PCR) [29].
• As a result of the present study, salvage treatment in patients enrolled in the GIMEMA trial AIDA is now anticipated at the time of molecular relapse, defined as the conversion to PCR positivity in two successive BM samplings during follow-up [18].
• The studies investigated chemotherapy alone (LAP0389) versus RA plus chemotherapy (AIDA) [30].
• We show by wheat germ agglutinin chromatography and galactosyl-transferase labelling that this p53 is O-glycosylated, and that at least one of the sugar residues masks the PAb421 epitope, as demonstrated by recovery of reactivity with PAb421 after digestion of Western blots of EB-1 cell extract with hexosaminidase [19].
• In situ Fourier transform infrared (FTIR) extinction spectra of airborne alpha-NAD microparticles generated by two different methods were recorded in the large coolable aerosol chamber AIDA of Forschungszentrum Karlsruhe [31].

References