Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.10.2 (focal adhesion kinase)
 44,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty different fractions of hematoporphyrin derivatives (HpD) and eight fractions of an HpD dimer mixture were isolated utilizing isocratic reversed-phase ion-pair high-performance liquid chromatography. These fractions were characterized by UV-visible and fluorescence spectrophotometry. Fluorescence quantum yields and photokill efficiency for each fraction in PTK2 epithelial cells were obtained. Results indicate that some part of the photoactivity exhibited by HpD may be due to impurities present in the HpD starting material, hematoporphyrin-IX dihydrochloride, depending on its source. It was also found that hematoporphyrin D, a commercial acetylated product formed during synthesis of HpD, contained a higher percentage of monomers than would be expected.
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PMID:Isolation and photodynamic effects of hematoporphyrin derivative components: a chromatographic analysis of the starting materials. 758 6

Focal adhesion kinase (pp125FAK or FAK) is a cytoplasmic protein-tyrosine kinase stimulated in response to cell interactions with extracellular matrix components and by exposure to a variety of agonists, including neuropeptides. FAK lacks Src-homology SH2 and SH3 domains, is highly conserved across species, and may represent the prototype for a tyrosine kinase family involved in novel signal transduction pathways. We have identified sequence variants in the 3' untranslated regions of the focal adhesion kinase gene in mice and used a PCR-based oligonucleotide hybridization assay to map the mouse gene (Fadk) to Chromosome (Chr) 15 distal to the myelocytomatosis protooncogene (Myc). The human homolog (PTK2) has been assigned to human Chr 8 on a panel of somatic hybrid cell lines. On the basis of synteny of mouse and human chromosomal maps, the position of the human PTK2 gene probably corresponds to human Chr 8q24-qter.
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PMID:Mapping of the focal adhesion kinase (Fadk) gene to mouse chromosome 15 and human chromosome 8. 776 95

A pulsed-laser microbeam at 532 nm wavelength (optical scissors) and a laser-induced optical trap at 1064 nm wavelength (optical tweezers) have been successively combined to dissect and manipulate chromosomes in live newt lung epithelial cells. These preliminary experimental results demonstrated that chromosome fragments dissected by laser microbeam surgery, regardless of their size, could be easily pulled or rotated by optical forces when positioned at the periphery of the mitotic spindle. In addition, chromosome arms which were not subjected to laser microsurgery also could be moved with the optical tweezers at the spindle periphery. In our previous study on rat kangaroo kidney cells (PTK2), this degree of facilty in manipulating chromosome movement was not possible, most likely due to the close proximity of the intermediate filament "cage" to the spindle. It is concluded herein that optical scissors and tweezers can be used in combination to study the interaction of chromosomes with the mitotic spindle in cells where the peripheral regions of the spindle are unobstructed by intermediate filaments. This can be performed on newt cells, where the diameter of the cage can be substantially larger than the diameter of the spindle.
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PMID:Directed movement of chromosome arms and fragments in mitotic newt lung cells using optical scissors and optical tweezers. 802 Jun 4

We have isolated a new gene (PTK2) which restores spermine uptake of a polyamine uptake-deficient mutant of Saccharomyces cerevisiae (Kakinuma, Y., Maruyama, T., Nozaki, T., Wada, Y., Oshumi, Y., and Igarashi, K., 1995, Biochem, Biophys. Res. Commun. 216, 985-992). In magnesium-limited medium, the cell growth of a spermine-sensitive polyamine uptake mutant transformed with PTK2 recovered its sensitivity to spermine. The nucleotide sequence of the PTK2 gene indicated that it is identical with the YJR059W open reading frame of chromosome X encoding a putative serine/threonine protein kinase. The deduced amino acid sequence of the PTK2 gene product was 38% identical and 55% similar with that of the PTK1 (POT1) gene product, a putative serine/threonine protein kinase, which was found to enhance spermine uptake of the same mutant. The results indicate that polyamine transport of yeast is regulated by multiple phosphorylation/dephosphorylation pathways.
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PMID:A second gene encoding a putative serine/threonine protein kinase which enhances spermine uptake in Saccharomyces cerevisiae. 892 Sep 34

The present investigation has been undertaken to examine the possibility that the cell nucleus, and specifically the genetic material, is a target site for photodynamic therapy. PTK2 and Hep-2 cells are pretreated with a medium containing 15 microg/ml (0.09 mM) 5-aminolevulinic acid (ALA). Individual fluorescence images are recorded for each selected cell using a cooled charge-coupled device (CCD). A laser microbeam system generating 630 nm is used for subcellular-region irradiation of specific targets: chromosomes, the mitotic spindle, the perispindle region and the peripheral cytoplasm. Nuclei of interphase cells are also irradiated. Data comparing the sensitivities of the different subcellular microirradiation sites in ALA-treated mitotic cells demonstrate that under the irradiation conditions used, the chromosome is the most sensitive subcellular target followed by the perispindle region, the peripheral cytoplasm and spindle, and, lastly, the interphase nucleus.
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PMID:Chromosomes are target sites for photodynamic therapy as demonstrated by subcellular laser microirradiation. 1083 49

The regulation of electrical membrane potential is a fundamental property of living cells. This biophysical parameter determines nutrient uptake, intracellular potassium and turgor, uptake of toxic cations, and stress responses. In fungi and plants, an important determinant of membrane potential is the electrogenic proton-pumping ATPase, but the systems that modulate its activity remain largely unknown. We have characterized two genes from Saccharomyces cerevisiae, PTK2 and HRK1 (YOR267c), that encode protein kinases implicated in activation of the yeast plasma membrane H(+)-ATPase (Pma1) in response to glucose metabolism. These kinases mediate, directly or indirectly, an increase in affinity of Pma1 for ATP, which probably involves Ser-899 phosphorylation. Ptk2 has the strongest effect on Pma1, and ptk2 mutants exhibit a pleiotropic phenotype of tolerance to toxic cations, including sodium, lithium, manganese, tetramethylammonium, hygromycin B, and norspermidine. A plausible interpretation is that ptk2 mutants have a decreased membrane potential and that diverse cation transporters are voltage dependent. Accordingly, ptk2 mutants exhibited reduced uptake of lithium and methylammonium. Ptk2 and Hrk1 belong to a subgroup of yeast protein kinases dedicated to the regulation of plasma membrane transporters, which include Npr1 (regulator of Gap1 and Tat2 amino acid transporters) and Hal4 and Hal5 (regulators of Trk1 and Trk2 potassium transporters).
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PMID:Regulation of yeast H(+)-ATPase by protein kinases belonging to a family dedicated to activation of plasma membrane transporters. 1100 61

Sky1p and Ptk2p are protein kinases that regulate ion transport across the plasma membrane of Saccharomyces cerevisiae. We show here that deletion of SKY1 or PTK2 in trk1,2Delta cells increase spermine tolerance, implying Trk1,2p independent activity. Unexpectedly, trk1,2Deltasky1Delta and trk1,2Deltaptk2Delta cells display hypersensitivity to LiCl. These cells also show increased tolerance to low pH and improved growth in low K(+), as demonstrated for deletion of PMP3 in trk1,2Delta cells. We show that Sky1p and Pmp3p act in different pathways. Hypersensitivity to LiCl and improved growth in low K(+) are partly dependent on the Nha1p and Kha1p antiporters and on the Tok1p channel. Finally, Dhh1p, a RNA helicase was demonstrated to improve growth of trk1,2Deltasky1Delta cells in low K(+). Overexpression of Dhh1p improves the ability of trk1,2Delta cells to grow in low K(+) while dhh1Delta cells are sensitive to spermine and salt ions. A model that integrates these results to explain the mechanism of ion transport across the plasma membrane is proposed.
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PMID:Deletions of SKY1 or PTK2 in the Saccharomyces cerevisiae trk1Deltatrk2Delta mutant cells exert dual effect on ion homeostasis. 1213 13

We prepare an extract of dog urine (DLU) that, when applied to monolayers of MDCK cells (epithelial, derived from a normal dog), enhances the transepithelial electrical resistance (TER) in a dose-dependent manner. This increase is not reflected in variations of the linear amount of TJ nor in changes of the pattern of junctional strands as observed in freeze fracture replicas, nor in the distribution of claudin 1 (a membrane protein of the TJ) nor ZO-1 (a TJ-associated protein). A preliminary characterization of the active component of DLU indicates that it weighs 30-50 kDa, bears a net negative electric charge, and is destroyed by type I protease but not by 10-min boiling. DLUs prepared from human, dog, rabbit and cat are effective on MDCK cells. However, dog DLU increases TER in MDCK (dog) as well as LLCPK1 (pig) monolayers, but not in other epithelial cell lines such as LLCRK1 (rabbit), PTK2 (kangaroo) and MA-104 (monkey), nor in the endothelial cell line CPA47 (cow). Given that in its transit from the glomerulus to the urinary bladder the filtrate increases its concentration by more than two orders of magnitude, the substance(s) we report may act at increasingly higher concentrations in each segment, and afford a potential clue to the progressive increase of TER across the walls of the nephron from the proximal to the collecting duct.
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PMID:Tight junctions are sensitive to peptides eliminated in the urine. 1217 45

We investigated 39 primary hepatocellular carcinomas (HCCs) for aberrations in DNA copy number, using comparative genomic hybridization (CGH). Gain of DNA at 8q was common in these tumors; high-level gains, indicative of gene amplification, occurred most frequently at 8q23-q24. Gains of 8q correlated with large (>5 cm) tumor size. To identify targets of the amplification events involving 8q, we determined expression levels of 14 candidate genes within that region in a total of 41 HCCs by means of real-time quantitative reverse-transcription polymerase chain reactions (RT-PCR). Significant correlation was found between elevated levels of expression and increases in copy number for PTK2 (located at 8q24.3) and EIF3S3 (at 8q23.3), but for none of the other candidates, which included MYC (8q24.1). Southern blot analyses confirmed that PTK2 and EIF3S3 were amplified, respectively, in 5 (19%) and 7 (26%) of the 27 tumors examined in accordance with expression patterns, an indication that expression of PTK2 and EIF3S3 was probably up-regulated by the amplification mechanism. When we analyzed potential relationships between elevated expression of PTK2 and EIF3S3 and clinicopathologic parameters, high expression of the 2 transcripts was significantly associated with large (>5 cm) tumor size and with hepatitis B virus (HBV) infection. In conclusion, PTK2 and EIF3S3, which, respectively, encode focal adhesion kinase and the p40 subunit of the eukaryotic initiation factor 3, were probable targets within the amplification at 8q23-q24 and may be involved in progression of HCC.
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PMID:PTK2 and EIF3S3 genes may be amplification targets at 8q23-q24 and are associated with large hepatocellular carcinomas. 1457 63

Glioblastomas frequently carry mutations in the PTEN tumor suppressor gene on 10q23.3. The tumor suppressor properties of Pten are closely related to its inhibitory effect on the phosphatidyl-inositol-3'-kinase (Pi3k)-dependent activation of protein kinase B (Akt) signalling. Here, we report on the analysis of 17 genes related to the Pi3k/Akt signalling pathway for genetic alteration and aberrant expression in a series of 103 glioblastomas. Mutation, homozygous deletion or loss of expression of PTEN was detected in 32% of the tumors. In contrast, we did not find any aberrations in the inositol polyphosphate phosphatase like-1 gene (INPPL1), whose gene product may also counteract Pi3k-dependent Akt activation. Analysis of genes encoding proteins that may activate the pathway upstream of Pi3k revealed variable fractions of tumors with EGFR amplification (31%), PDGFRA amplification (8%), and IRS2 amplification (2%). The protein tyrosine kinase 2 (PTK2/FAK1) gene was neither amplified nor overexpressed at the mRNA level. Investigation of three genes encoding catalytic subunits of Pi3k (PIK3CA, PIK3CD, and PIK3C2B) revealed amplification of PIK3C2B (1q32) in 6 tumors (6%). Overexpression of PIK3C2B mRNA was detected in 4 of these cases. PIK3CD (1p36.2) and PIK3CA (3q26.3) were not amplified but PIK3CD mRNA was overexpressed in 6 tumors (6%). Amplification and overexpression of AKT1 was detected in a single case of gliosarcoma. The IRS1, PIK3R1, PIK3R2, AKT2, AKT3, FRAP1, and RPS6KB1 genes were neither amplified nor overexpressed in any of the tumors. Taken together, our data indicate that different genes related to the Pi3k/Akt signalling pathway may be aberrant in glioblastomas.
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PMID:Genetic alterations and aberrant expression of genes related to the phosphatidyl-inositol-3'-kinase/protein kinase B (Akt) signal transduction pathway in glioblastomas. 1465 56


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