Disease relevance of Serpinb1a

• Brain cells from murine embryos were transfected with the polyoma virus large T or the adenovirus 5 EIA gene and, simultaneously, with the phosphotransferase coding NeoR gene [1].
• This requires the rapid entry of c-Fos into specific AP-1 DNA-binding complexes and can be strongly inhibited by the adenovirus EIA 12S gene product [2].
• Therefore, in this study, we asked (a) whether EIA might sensitize response to paclitaxel in human HER-2/neu-overexpressing ovarian cancer cells, and, if so, what is the mechanism responsible; and (b) whether this enhanced chemosensitivity would translate into a therapeutic effect in an ovarian cancer xenograft model [3].
• Four murine cellular tumor models expressing various combinations of oncogenes (SV40 large T and v-Ha-ras, SV40 large T and v-src, SV40 large T and neu, adenovirus EIA and v-Ha-ras) induce sarcoma when they are inoculated s.c. into the DBA/2 syngenic mice [4].
• All the tumor cell lines except EIA-ras, induce massive overt artificial metastases principally in the lung after i.v. injection [4].

High impact information on Serpinb1a

• Furthermore, when transgenic mice bearing 250 EI genes and mice bearing 7 copies of an EI enhancer-directed human growth hormone (hGh) gene were mated to produce mice with two unlinked arrays of EI enhancer-driven transgenes, each array was transcribed at the same rate as in mice bearing each array separately [5].
• This decrease was not due to a titration of essential transcription factors, because transgenic mice with as many as 250 copies of the rat EI enhancer continued transcription of the endogenous mouse EI gene at its normal rate [5].
• The rat elastase I (EI) regulatory region is an enhancer that directs efficient pancreas-specific transcription of linked genes integrated in the chromosomes of transgenic mice [5].
• Antibodies PI1 and PI2 were redistributed independently during prophase, and dispersed into the cytoplasm during prometaphase [6].
• The transcriptional enhancer of the EI gene, from nucleotides -205 to -72, recapitulates the expression of the endogenous gene in transgenic mice; it directs not only pancreatic acinar cell expression of a human growth hormone (hGH) transgene but also expression to the stomach, duodenum, and colon [7].

Chemical compound and disease context of Serpinb1a

• Moreover, alpha,beta-Me-ATP (3 microg/rat, i.t.) induced hyperalgesia in tail flick test, but it was prevented by co-injection of alpha,beta-Me-ATP with suramin (120 microg/rat, i.t.) or TFG extract (1mg/rat, i.t.). Effective concentrations of TFG extract in the above mentioned experiments did not inhibit COX enzymes in EIA tests [8].

Biological context of Serpinb1a

• However, with increasing numbers of tandemly repeated EI transgenes, the transcription rate per gene decreased [5].
• In this study, we utilized a panel of E1A mutants deficient in cellular protein binding to analyse the molecular basis for EIA inhibition of a minimal, c-Fos-dependent TF promoter/ reporter construct in mouse AKR-2B fibroblasts [2].
• In mice, the zwitterionic detergent-extracted HSV-1 antigen preparation elicited an EIA antibody response and partial protection against homologous virus challenge [9].
• The main features of the methodology are: RNA competitors which control for all aspects of the process from RNA extraction, through reverse transcription (RT) and PCR amplification; a general cloning vector, pQPCR1, for building RNA competitors that does not require prior analyte cDNA cloning; and analysis by plate based EIA [10].
• Possible immunological cross-reactions between enterovirus proteins and heat shock proteins were studied by EIA and immunoblotting by using purified virus preparations, viral expression proteins VP1 and VP0, and recombinant HSP60/65 proteins, and corresponding polyclonal antisera [11].

Anatomical context of Serpinb1a

• Excised segments of colon from CD mice were immersed in synthetic interstitial fluid (SIF) exposing the serosal surface during 5 min to different types of noxious stimuli; the increase in neuropeptide and PGE(2) release were analyzed (by EIA technique) [12].
• Using this assay and a previously described EIA for AcSDKP, a negative regulator of pluripotent haematopoietic stem cell proliferation, the levels of these two peptides were determined in mouse tissue extracts [13].
• METHODS: Hybrid cell clones were developed by immunization of mice with DU145 cells and tested for immunoreactivity by solid phase EIA and cytotoxicity in vitro on DU145 in the presence of the complement, employing colorimetric quantitation by MTS (3- (4-, 5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-(4-sulfophenyl)-2H-tetrazolium) [14].
• Hybridomas were produced which expressed monoclonal anti-soman antibodies as determined by microtiter enzyme-linked-antibody immunoassay (EIA) [15].
• The plasmas were centrifuged for 3 hr at 143,000 g and the antigenic activity of core-protein was studied in the pellets by EIA using four MABs able to recognize four nonoverlapping determinants, two at N-terminus and two at C-terminus of recombinant core (1-150 aa) [16].

Associations of Serpinb1a with chemical compounds

• Using DA-3 antibody, an indirect competitive enzyme immunoassay (idc-EIA) was developed for measurement of domoic acid [17].
• Enzyme expression was evaluated by immunoblotting, PGE2 by EIA, and NO by Griess reaction [18].
• Urinary excretion of albumin, determined by EIA, was remarkably increased in the 129/COX-2-/- (16.4 +/- 4.1 vs. 0.16 +/- 0.043 mg albumin/mg creatinine, P < 0.001), and to a lesser extent in the male C57/COX-2-/- mice (0.595 +/- 0.416 vs. 0.068 +/- 0.019) [19].
• Prostaglandin E2 (PGE2) and leukotriene C4 (LTC4) were determined by EIA analysis [20].
• Th HA cells were cultured under conditions for maximum Fc alpha R expression, were added to individual wells of 96-well EIA plates, and were fixed in situ with glutaraldehyde [21].

Analytical, diagnostic and therapeutic context of Serpinb1a

• One of them, 52-DH1 (DH), reacted exclusively with cFns but not with plasma Fns (pFns) in immunoblotting and solid-phase EIA [22].
• Serum levels of corticosterone and urinary levels of biopyrrins were determined by EIA and ELISA, respectively [23].
• Simultaneous quantitation of multiple cytokine mRNAs by RT-PCR utilizing plate based EIA methodology [10].
• Anti-HBs levels were measured by RIA and expressed in IU l-1; anti-pre-S2 response was evaluated by both EIA and Western blot analysis [24].
• Using immunofluorescence, EIA and immunoblot analyses, we failed to identify induction of autoantibodies following vaccination with gB, whether administered alone as a purified protein subunit with adjuvant, or in combination with expression in a vectored approach using a recombinant canarypox [25].

References