排序方式: 共有16条查询结果,搜索用时 381 毫秒
1.
EA Dukhanina TI Lukyanova EA Romanova V Guerriero NV Gnuchev GP Georgiev DV Yashin LP Sashchenko 《Cell cycle (Georgetown, Tex.)》2015,14(22):3635-3643
PGRP-S (Tag7) is an innate immunity protein involved in the antimicrobial defense systems, both in insects and in mammals. We have previously shown that Tag7 specifically interacts with several proteins, including Hsp70 and the calcium binding protein S100A4 (Mts1), providing a number of novel cellular functions. Here we show that Tag7–Mts1 complex causes chemotactic migration of lymphocytes, with NK cells being a preferred target. Cells of either innate immunity (neutrophils and monocytes) or acquired immunity (CD4+ and CD8+ lymphocytes) can produce this complex, which confirms the close connection between components of the 2 branches of immune response. 相似文献
2.
Coding sequence composition flanking either signal element alters V(D)J recombination efficiency. 总被引:6,自引:1,他引:5 下载免费PDF全文
Lymphoid V(D)J rearrangement is targeted by recombination signal sequences (RSS) bordering V, D or J exons. We demonstrate that the DNA composition of flanking coding positions, particularly poly(A) or poly(T) stretches at one or both RSS, diminishes V(D)J recombination up to 100-fold. Positionally correct cleavages occur in the inhibited reactions, since the junctions formed show the same frequency of precision as uninhibited reactions. Open/shut cleavage/rejoining is not increased at a normal RSS in substrates containing inhibitory A/T homopolymers versus random sequence at a second RSS. Thus recombinase action at both cleavage sites is severely disrupted by modified coding sequences. 相似文献
3.
scid cells are deficient in Ku and replication protein A phosphorylation by the DNA-dependent protein kinase. 总被引:8,自引:3,他引:5 下载免费PDF全文
Cell mutants of the Ku nuclear DNA-binding complex are ionizing radiation sensitive and show V(D)J recombination defects. Ku binds and activates a catalytic subunit of DNA-dependent protein kinase (DNA-PK), although the substrates for DNA-PK are unknown. We found that scid cell extracts were deficient in Ku phosphorylation by DNA-PK. Human chromosome 8-complemented scid cells, containing the human DNA-PK catalytic subunit, restored Ku phosphorylation. Likewise, radiation-induced RPA hyperphosphorylation was not completed in scid cells compared with control or chromosome 8-reconstituted cells. Thus, the inactivity of DNA-PK is likely responsible for the repair and recombination defects in scid cells. 相似文献
4.
Requirement for the kinase activity of human DNA-dependent protein kinase catalytic subunit in DNA strand break rejoining 总被引:16,自引:0,他引:16 下载免费PDF全文
Kurimasa A Kumano S Boubnov NV Story MD Tung CS Peterson SR Chen DJ 《Molecular and cellular biology》1999,19(5):3877-3884
The catalytic subunit of DNA-dependent protein kinase (DNA-PKcs) is an enormous, 470-kDa protein serine/threonine kinase that has homology with members of the phosphatidylinositol (PI) 3-kinase superfamily. This protein contributes to the repair of DNA double-strand breaks (DSBs) by assembling broken ends of DNA molecules in combination with the DNA-binding factors Ku70 and Ku80. It may also serve as a molecular scaffold for recruiting DNA repair factors to DNA strand breaks. This study attempts to better define the role of protein kinase activity in the repair of DNA DSBs. We constructed a contiguous 14-kb human DNA-PKcs cDNA and demonstrated that it can complement the DNA DSB repair defects of two mutant cell lines known to be deficient in DNA-PKcs (M059J and V3). We then created deletion and site-directed mutations within the conserved PI 3-kinase domain of the DNA-PKcs gene to test the importance of protein kinase activity for DSB rejoining. These DNA-PKcs mutant constructs are able to express the protein but fail to complement the DNA DSB or V(D)J recombination defects of DNA-PKcs mutant cells. These results indicate that the protein kinase activity of DNA-PKcs is essential for the rejoining of DNA DSBs in mammalian cells. We have also determined a model structure for the DNA-PKcs kinase domain based on comparisons to the crystallographic structure of a cyclic AMP-dependent protein kinase. This structure gives some insight into which amino acid residues are crucial for the kinase activity in DNA-PKcs. 相似文献
5.
V(D)J recombination coding junction formation without DNA homology: processing of coding termini. 总被引:9,自引:5,他引:4 下载免费PDF全文
Coding junction formation in V(D)J recombination generates diversity in the antigen recognition structures of immunoglobulin and T-cell receptor molecules by combining processes of deletion of terminal coding sequences and addition of nucleotides prior to joining. We have examined the role of coding end DNA composition in junction formation with plasmid substrates containing defined homopolymers flanking the recombination signal sequence elements. We found that coding junctions formed efficiently with or without terminal DNA homology. The extent of junctional deletion was conserved independent of coding ends with increased, partial, or no DNA homology. Interestingly, G/C homopolymer coding ends showed reduced deletion regardless of DNA homology. Therefore, DNA homology cannot be the primary determinant that stabilizes coding end structures for processing and joining. 相似文献
6.
7.
8.
We present an efficient computational architecture designed using supervised machine learning model to predict amyloid fibril
forming protein segments, named AmylPepPred. The proposed prediction model is based on bio-physio-chemical properties of
primary sequences and auto-correlation function of their amino acid indices. AmylPepPred provides a user friendly web interface
for the researchers to easily observe the fibril forming and non-fibril forming hexmers in a given protein sequence. We expect that
this stratagem will be highly encouraging in discovering fibril forming regions in proteins thereby benefit in finding therapeutic
agents that specifically aim these sequences for the inhibition and cure of amyloid illnesses.
Availability
AmylPepPred is available freely for academic use at www.zoommicro.in/amylpeppred 相似文献9.
10.
Identification of drm, a novel gene whose expression is suppressed in transformed cells and which can inhibit growth of normal but not transformed cells in culture. 总被引:3,自引:0,他引:3 下载免费PDF全文
L Z Topol M Marx D Laugier N N Bogdanova N V Boubnov P A Clausen G Calothy D G Blair 《Molecular and cellular biology》1997,17(8):4801-4810
Using differential display analysis, we compared the expression of RNA in v-mos-transformed cells and their flat revertant and isolated a novel gene, drm (down-regulated in mos-transformed cells), whose expression is down-regulated in parental v-mos-transformed cells but which is expressed at a high level in the revertant and normal rat fibroblasts (REF-1 cells). Analysis of different oncogene-transformed cells revealed that drm gene expression was also suppressed in REF-1 cells transformed by v-ras, v-src, v-raf, and v-fos. The drm cDNA contains a 184-amino-acid-protein-encoding open reading frame which shows no significant homologies to known genes in DNA databases. Polyclonal antibodies raised against drm peptide detect a protein with the predicted size of 20.7 kDa in normal cells and under nonpermissive conditions in cells conditionally transformed by v-mos but not in parental v-mos-transformed cells. Northern analysis of normal adult tissues shows that drm is expressed as a 4.4-kb message in a tissue-specific manner, with high expression in the brain, spleen, kidney, and testis and little or no expression in the heart, liver, and skeletal muscle. In situ hybridization analysis in adult rat tissue reveals good correlation with this pattern and indicates that drm mRNA is most highly expressed in nondividing and terminally differentiated cells, such as neurons, type 1 lung cells, and goblet cells. Transfection of a drug-selectable drm expression vector dramatically reduced the efficiency of colony formation in REF-1 and CHO cells, and the drm-transfected REF-1 survivors expressed low or nondetectable levels of exogenous drm mRNA. The toxic effects of drm can be overcome by cotransfection with constructs expressing oncogenic ras; furthermore, cells expressing high levels of drm and conditionally transformed with mos-expressing Moloney murine sarcoma virus rapidly undergo apoptosis when shifted to the nonpermissive temperature. Taken together, our data suggest that cells expressing high levels of drm undergo apoptotic death in the absence of oncogene-induced transformation and that drm represents a novel gene with potential roles in cell growth control or viability and tissue-specific differentiation. 相似文献