Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.7.13.3 (
histidine kinase
)
2,405
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
HK1
.4 mAb was identified based on its ability to stimulate proliferation of cloned murine CTL. Within the lymphoid lineage, mAb
HK1
.4 bound exclusively to CTL, regardless of the expression of Lyt-2 or MHC restriction.
HK1
.4 mAb also bound to 40% of bone marrow cells and less than 5% of thymocytes from all mouse strains tested. Based on the tissue distribution of the determinant with which it reacted and the ability to cross-block binding of the anti-Ly-6 mAb H9/25, mAb
HK1
.4 appeared to react with a product of the Ly-6 locus. However, significant differences were observed between the properties of mAb
HK1
.4 and other, previously described anti-Ly-6 mAb. Cell proliferation and lymphokine release by cloned CTL were stimulated by culture with mAb
HK1
.4 alone or in the presence of non-stimulatory levels of IL-2. This proliferation and lymphokine release were not blocked by the addition of soluble anti-Lyt-2 or anti-IL-2R mAb. Activation induced by
HK1
.4 mAb proceeds in the absence of accessory cells, of cross-linking of the TCR, or the addition of mitogens or PMA. Stimulation of cells by anti-TCR mAb was not blocked by the addition of soluble
HK1
.4 mAb, and the stimulatory effects of
HK1
.4 and anti-TCR mAb were not additive. However, IL-2-driven proliferation of CTL clones was dramatically inhibited by the addition of
HK1
.4 mAb.
HK1
.4 mAb had no effect on Ag-specific or
lectin
-facilitated cytolysis. Taken together, these data indicate that mAb
HK1
.4 operates via an IL-2-independent pathway of activation that is also independent of the TCR.
...
PMID:Characterization of an anti-Ly-6 monoclonal antibody which defines and activates cytolytic T lymphocytes. 325 67
To understand the mechanisms of aluminum (Al) tolerance in wheat (Triticum aestivum L.), suppression subtractive hybridization (SSH) libraries were constructed from Al-stressed roots of two near-isogenic lines (NILs). A total of 1,065 putative genes from the SSH libraries was printed in a cDNA array. Relative expression levels of those genes were compared between two NILs at seven time points of Al stress from 15 min to 7 days. Fifty-seven genes were differentially expressed for at least one time point of Al treatment. Among them, 28 genes including genes for aluminum-activated malate transporter-1, ent-kaurenoic acid oxidase-1, beta-glucosidase,
lectin
,
histidine kinase
, and phospoenolpyruvate carboxylase showed more abundant transcripts in Chisholm-T and therefore may facilitate Al tolerance. In addition, a set of genes related to senescence and starvation of nitrogen, iron, and sulfur, such as copper chaperone homolog, nitrogen regulatory gene-2, yellow stripe-1, and methylthioribose kinase, was highly expressed in Chisholm-S under Al stress. The results suggest that Al tolerance may be co-regulated by multiple genes with diverse functions, and those genes abundantly expressed in Chisholm-T may play important roles in enhancing Al tolerance. The down-regulated genes in Chisholm-S may repress root growth and restrict uptake of essential nutrient elements, and lead to root senescence.
...
PMID:Transcriptional analysis between two wheat near-isogenic lines contrasting in aluminum tolerance under aluminum stress. 1703 77