Disease relevance of Lymphocytes, Null

• Differences in purine metabolizing enzyme activities in human leukemia T-cell, B-cell and null cell lines [1].
• Elevated adenosine deaminase and purine nucleoside phosphorylase activity in peripheral blood null lymphocytes from patients with acquired immune deficiency syndrome [2].
• A mouse model of TSC1 reveals sex-dependent lethality from liver hemangiomas, and up-regulation of p70S6 kinase activity in Tsc1 null cells [3].
• The level of uridine kinase activity in the feline lymphosarcoma of thymus-dependent lymphocyte orgin and childhood lymphocytic leukemia of possible thymus-dependent lymphocyte or null-cell origin was similar to the induced level in phytohemagglutinin-stimulated normal lymphocytes, i.e., thymus-dependent lymphocytes [4].
• Although Aag null cells are sensitive to MMC-induced growth delay and cell cycle arrest, their sensitivity is modest compared to that of Fanconi anemia cells [5].

High impact information on Lymphocytes, Null

• Significantly, hypoxia-induced HIF1alpha expression was completely inhibited in Siah1a/2 null cells, yet could be rescued upon inhibition of PHD3 by RNAi [6].
• Compared with wild-type MEFs, p16Ink4a-null MEFs exhibited an increased rate of immortalization, although this rate was less than that observed previously for cells null for Ink4a/Arf, p19Arf or p53 (refs 4, 5) [7].
• When the class II null cell line 721.174 was transfected with class II DR3 genes, DR molecules were produced in normal amounts [8].
• Thus, cad and gadd45 are the only proposed targets of c-Myc that may contribute to the dramatic slow growth phenotype of c-myc null cells [9].
• c-myc null cells misregulate cad and gadd45 but not other proposed c-Myc targets [9].

Chemical compound and disease context of Lymphocytes, Null

• Levamisole was shown to alter antibody responses to tetanus and typhoid antigens, lymphocyte blastogenesis to phytohemagglutinins, and the number of null cells in peripheral blood [10].
• To study the relationship between null cell adenomas, oncocytomas and gonadotroph adenomas, we analyzed 32 surgically removed formalin-fixed paraffin-embedded pituitary tumors for the expression of pituitary hormone messenger RNAs (mRNAs) by in situ hybridization (ISH) [11].
• Thus, we conclude that null cell adenomas and oncocytomas contain cells that can produce pituitary glycoprotein hormones, and that the majority produce gonadotropins [12].
• After treatment with phorbol 12-myristate 13-acetate (10(-7) M) for 7 days, there was an increase in the mRNA for CgB and SgII mRNAs in GH and null cell tumors, while dexamethasone treatment for 7 days increased CgA mRNA in GH and null cell adenomas [13].
• These results indicate that immunohistochemically characterized null cell adenomas as well as normal pituitaries express dopamine receptors, but that the binding sites in null cell adenomas are much less those in PRL-secreting adenomas [14].

Biological context of Lymphocytes, Null

• In Suv39h double null cells, pericentric heterochromatin is converted to alternative methylation imprints and accumulates H3-K27 trimethylation and H3-K9 monomethylation [15].
• Reconstitution of the complete tetrameric Fc epsilon RI receptor, lyn and syk in a non-hematopoietic 'null' cell line is sufficient to reconstruct clustering-controlled receptor tyrosine phosphorylation and activation of syk, without apparent requirement for hematopoietic specific phosphatases [16].
• Analysis of Rat1 c-myc null cells shows these same death stimuli induce apoptosis with characteristic features of nuclear condensation, membrane blebbing, poly (ADP-ribose) polymerase cleavage, and DNA fragmentation; however, this Myc-independent apoptosis is not inhibited by Bcl-2 [17].
• We showed that rad12 null cells are sensitive to DNA damage induced by UV light and gamma radiation, as well as to the DNA synthesis inhibitor hydroxyurea [18].
• This analysis demonstrated that F96-224 cells show delayed cell death when compared with rapid growth arrest of an Artemis null cell line, and the emergence of a cycling population shown by a control line [19].

Anatomical context of Lymphocytes, Null

• We demonstrate here that mice chimeric for wild-type and PPAR gamma null cells show little or no contribution of null cells to adipose tissue, whereas most other organs examined do not require PPAR gamma for proper development [20].
• Immunofluorescent studies with fluoresceinated anti-brain sera demonstrated acquisition of T-cell surface antigens by BM null lymphocytes during the blastogenic response of this tissue to PHA [21].
• The cultured TdT+ cells are antigenically "null" cells that further resemble their normal counterparts in bone marrow with respect to morphology, size, cortisone sensitivity, and pattern of TdT fluorescence [22].
• By using monoclonal antibodies, we found that this patient's granulocytes, monocytes, and null cells were deficient in Mo1 (equivalent to OKM1 and Mac-1), a cell surface molecule consisting of two noncovalently linked glycoproteins of 155,000 and 94,000 D [23].
• Thymosin-induced reduction of "null cells" in peripheral-blood lymphocytes of patients with systemic lupus erythematosus [24].

Associations of Lymphocytes, Null with chemical compounds

• All these events are abolished in Med1/Trap220 null cells, indicating a key role for TRAP/Mediator in these processes [25].
• Compensatory prostaglandin E2 biosynthesis in cyclooxygenase 1 or 2 null cells [26].
• Cultured leukemic T and null lymphocytes are highly sensitive to growth inhibition by thymidine, as well as the other deoxynucleosides, deoxyguanosine and deoxyadenosine [27].
• RacB activation is partly controlled by the PI3K pathway. pi3k1/2 null cells and wild-type cells treated with LY294002 exhibit a significantly reduced second peak of RacB activation, which is linked to pseudopod extension, whereas a PTEN hypomorph exhibits elevated RacB activation [28].
• We have disrupted an inositol 1,4,5-trisphosphate (InsP(3)) receptor-like gene, iplA, to produce null cells in which Ca(2+) entry in response to chemoattractants is abolished, as is the normal increase in free cytosolic Ca(2+) ([Ca(2+)](c)) that follows chemotactic stimulation [29].

Gene context of Lymphocytes, Null

• Consistent with these data, cyclin G null cells have both Mdm2 that is hyperphosphorylated at T216 and markedly higher levels of p53 protein when compared to wild-type cells [30].
• We show that nuclear beta-catenin expression is constitutively elevated in PTEN null cells and this elevated expression is reduced upon reexpression of PTEN [31].
• Finally, Rb removal induced no DNA synthesis even in pocket-protein null cells [32].
• Cells homozygous mutant for mRpL12 have reduced mitochondrial activity, and exhibit growth defects that are very similar to those of cdk4 null cells [33].
• In addition, numerous aggregates of myosin heavy chain accumulate in the sqh null cells [34].

Analytical, diagnostic and therapeutic context of Lymphocytes, Null

• Analysis of the surface immunoglobulins of null cells by radioimmunoassay and polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate suggested that they are 1) qualitatively similar to those of B cells and 2) present in amounts between 10 and 30% of those of B cells [35].
• Myosin IIB null cells displayed multiple unstable and disorganized protrusions, although they were still able to generate a large fraction of traction forces when cultured on flexible polyacrylamide substrates [36].
• Rabbit antisera with activity directed against p28 (alpha-ATC) were prepared and p28 was identified by immunoprecipitation in NP-40 extracts of activated, extrinsically labeled lymphocytes. p28 was not expressed in appreciable amounts by unstimulated T cells, stimulated or unstimulated B cells, null cells, or adherent cells [37].
• Here we use scanning electron microscopy, light microscopy, immunofluorescence and computer analysis of time-lapse video films to study how D. discoideum myosin null cells of strains HS2205 and HS2206 aggregate [38].
• The death defect in Bin1 null cells was significant insofar as it abolished FTI efficacy in tumor xenograft assays. p53 deletion did not phenocopy the effects of Bin1 deletion [39].

References