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1.
The purpose of this work was to study the genetic basis of histocompatibility antigens encoded by the mouse minor histocompatibility
(H) locusH-3. Both class I major histocompatibility complex (MHC)-restricted cytotoxic T lymphocytes (CTL) and class II MHC-restricted
helper T cells (TH) specific for antigens encoded by genes within theH-3 locus were isolated and analyzed. Typing a number of mouse strains for expression of antigens recognized by these TH and
CTL suggested that there was a different strain distribution pattern of expression of the antigens recognized by TH compared
with those recognized by CTL. Separation of the genes whose products stimulate TH from those whose products stimulate CTL
was suggested by: (1) analysis of the strain B10.FS(92NX)/Grf that has undergone recombination within theH-3 region; (2) genetic segregation studies of (B10.UW-H-3
b/Sn×C57BL/10Sn)F2 mice; and (3) F1 complementation studies in which CTL specific for products of the TH-defined gene(s) could not be detected, even in the absence
of immune responses to products of the CTL-defined genes. Taken together, these data suggest that in addition to two genes
(B2m andCd-1) within theH-3 region whose products typically stimulate class I MHC-restricted CTL, there is at least one additional gene whose product
selectively stimulates class II MHC-restricted TH. This new gene is located telomeric from the CTL-defined genes and between
the lociwe andun on chromosome 2. These data demonstrate a novel degree of complexity of theH-3 “locus” and suggest selective presentation of minor H gene products in the context of class I or class II MHC proteins. 相似文献
2.
Ralph J. Graff Michael E. Kurtz Robert Paul Danielle Martin Derry C. Roopenian 《Immunogenetics》1991,33(2):96-100
The purpose of this work was to elucidate the genetic fine structure of the central portion of mouse chromosome (Chr) 2. Seven Chr 2 congenic mouse strains [B10.PA(L)-pa we un a
t
, B10.PA(L)-pa A
w
, B10.PA(L)-we un a
t
, B10.PA(J)-pa a, B10.FS-we A
w
, B10.C-we A
w
, and B10.YBR-a] were produced. Breeding studies were carried out using strains B10.PA(L)-pa we un a
t
and B10.LP-H-13
b
to accurately determine the recombination frequencies between marker genes pa and we (1.9%±0.3), we and un (8.8%±0.5), and un and a
t
(4.5%±0.4) of strain B10.PA(L)-pa we un a
t
. These strains and other Chr 2 congenic strains were typed for immunologically defined loci using monoclonal antibody (mAb) C23 reactive with the gene product of B2m
b
T-lymphocyte clone C1 reactive with the gene product of H-3
a
and H-3
c
, and lymphocyte clone H1.8 reactive with the gene product of Hd-1
a
. B2m and H-3 typing located a recombinational event separating [pa B2m H-3] from we (the order of bracketed genes is not known). Hd-1 typing indicated that Hd-1 maps distal to [H-42, H-44] and proximal to un. The gene order [pa, B2m, H-3], we, [H-42, H-45], Hd-1, un, H-13, a
t
, with H-44 mapping centromeric to Hd-1, is indicated by the data.
Address correspondence and offprint requests to: R. J. Graff. 相似文献
3.
Soldati Adrian Muhumuza Geresomu Dezecache Guillaume Fedurek Pawel Taylor Derry Call Josep Zuberbühler Klaus 《International journal of primatology》2023,44(1):116-139
International Journal of Primatology - Observations of early vocal behaviours in non-human primates (hereafter primates) are important for direct comparisons between human and primate vocal... 相似文献
4.
F1 complementation results indicate that a new gene, putatively controlling a minor histocompatibility antigen, is closely linked to the minor histocompatibility gene, H-3, in the fifth linkage group of chromosome 2 of the mouse. This gene controls a product that was capable of inducing as well as acting as a target for cytotoxic lymphocytes (CTL). The lytic activity of CTL developed in B10.LP-H-3D mice specific for the product of the new gene of B10 was restricted to target cells possessing H-2Db antigens. This contrasts to the H-2Kb-restricted activity of H-3.1 specific CTL. 相似文献
5.
6.
Yuyang Sun Senthil Selvaraj Archana Varma Susan Derry Abe E. Sahmoun Brij B. Singh 《The Journal of biological chemistry》2013,288(1):255-263
TRPM7 is a novel magnesium-nucleotide-regulated metal current (MagNuM) channel that is regulated by serum Mg2+ concentrations. Changes in Mg2+ concentration have been shown to alter cell proliferation in various cells; however, the mechanism and the ion channel(s) involved have not yet been identified. Here we demonstrate that TRPM7 is expressed in control and prostate cancer cells. Supplementation of intracellular Mg-ATP or addition of external 2-aminoethoxydiphenyl borate inhibited MagNuM currents. Furthermore, silencing of TRPM7 inhibited whereas overexpression of TRPM7 increased endogenous MagNuM currents, suggesting that these currents are dependent on TRPM7. Importantly, although an increase in the serum Ca2+/Mg2+ ratio facilitated Ca2+ influx in both control and prostate cancer cells, a significantly higher Ca2+ influx was observed in prostate cancer cells. TRPM7 expression was also increased in cancer cells, but its expression was not dependent on the Ca2+/Mg2+ ratio per se. Additionally, an increase in the extracellular Ca2+/Mg2+ ratio led to a significant increase in cell proliferation of prostate cancer cells when compared with control cells. Consistent with these results, age-matched prostate cancer patients also showed a subsequent increase in the Ca2+/Mg2+ ratio and TRPM7 expression. Altogether, we provide evidence that the TRPM7 channel has an important role in prostate cancer and have identified that the Ca2+/Mg2+ ratio could be essential for the initiation/progression of prostate cancer. 相似文献
7.
To identify genes involved in programmed cell death (PCD) in Caenorhabditis elegans, we screened a comprehensive set of chromosomal deficiencies for alterations in the pattern of PCD throughout embryonic development. From a set of 58 deficiencies, which collectively remove approximately 74% of the genome, four distinct classes were identified. In class I (20 deficiencies), no significant deviation from wild type in the temporal pattern of cell corpses was observed, indicating that much of the genome does not contain zygotic genes that perform conspicuous roles in embryonic PCD. The class II deficiencies (16 deficiencies defining at least 11 distinct genomic regions) led to no or fewer-than-normal cell corpses. Some of these cause premature cell division arrest, probably explaining the diminution in cell corpse number; however, others have little effect on cell proliferation, indicating that the reduced cell corpse number is not a direct result of premature embryonic arrest. In class III (18 deficiencies defining at least 16 unique regions), an excess of cell corpses was observed. The developmental stage at which the extra corpses were observed varied among the class III deficiencies, suggesting the existence of genes that perform temporal-specific functions in PCD. The four deficiencies in class IV (defining at least three unique regions), showed unusually large corpses that were, in some cases, attributable to extremely premature arrest in cell division without a concomitant block in PCD. Deficiencies in this last class suggest that the cell death program does not require normal embryonic cell proliferation to be activated and suggest that while some genes required for cell division might also be required for cell death, others are not. Most of the regions identified by these deficiencies do not contain previously identified zygotic cell death genes. There are, therefore, a substantial number of as yet unidentified genes required for normal PCD in C. elegans. 相似文献
8.
Choi EY Yoshimura Y Christianson GJ Sproule TJ Malarkannan S Shastri N Joyce S Roopenian DC 《Journal of immunology (Baltimore, Md. : 1950)》2001,166(7):4370-4379
Minor histocompatibility Ags (minor H Ags) are substantial impediments to MHC-matched solid tissue and bone marrow transplantation. From an antigenic standpoint, transplantation between MHC-matched individuals has the potential to be remarkably complex. To determine the extent to which the immune response is simplified by the phenomenon of immunodominance, we used peptide/MHC tetramers based on recently discovered minor H Ags (H60, H13, and HY) and monitored in vivo CD8 T cell responses of female C57BL/6 mice primed with MHC-matched, but background-disparate, male BALB.B cells. CD8 T cells against H60 overwhelmed responses to the H13 and HY throughout primary and secondary challenge. H60 immunodominance was an inherent quality, overcoming a lower memory precursor frequency compared with that of H13 and evoking a T cell response with diverse TCRV beta usage. IFN-gamma staining examining congenically defined minor H Ags extended H60 dominance over additional minor H Ags, H28, H4, and H7. These four minor H Ags accounted for up to 85% of the CD8 T cell response, but H60 stood out as the major contributor. These findings show that immunodominance applies to antigenically complex transplantation settings in vivo and that the responses to the H60 minor H Ag dominates in this model. We suggest that immunodominant minor H Ags are those that result from the absence of a self analog. 相似文献
9.
10.
Yadav R Yoshimura Y Boesteanu A Christianson GJ Ajayi WU Shashidharamurthy R Stanic AK Roopenian DC Joyce S 《Journal of immunology (Baltimore, Md. : 1950)》2003,170(10):5133-5142
Minor histocompatibility (H) Ag disparities result in graft-vs-host disease and chronic solid allograft rejection in MHC-identical donor-recipient combinations. Minor H Ags are self protein-derived peptides presented by MHC class I molecules. Most arise as a consequence of allelic variation in the bound peptide (p) that results in TCR recognizing the p/MHC as foreign. We used a combinational peptide screening approach to identify the immune dominant H2K(b)-restricted epitope defining the mouse H4(b) minor H Ag. H4(b) is a consequence of a P3 threonine to isoleucine change in the MHC-bound peptide derived from epithelial membrane protein-3. This allelic variation also leads to phosphorylation of the H4(b) but not the H4(a) epitope. Further, ex vivo CD8(+) T lymphocytes bind phosphorylated Ag tetramers with high efficiency. Although we document the above process in the minor H Ag system, posttranslational modifications made possible by subtle amino acid changes could also contribute to immunogenicity and immune dominance in tumor immunotherapeutic settings. 相似文献