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V Likhite

Publications and source records attributed to V Likhite.

At least 19 recordsLinked to original sources
PubMed1999

Isolation of mouse TFIID and functional characterization of TBP and TFIID in mediating estrogen receptor and chromatin transcription.

TFIID is a general transcription factor required for the assembly of the transcription machinery on most eukaryotic promoters transcribed by RNA polymerase II. Although the TATA-binding subunit (TBP) of TFIID is able to support core promoter and activator-dependent transcription under some circumstances, the roles of TBP-associated factors (TAF(II)s) in TFIID-mediated activation remain unclear. To define the evolutionarily conserved function of TFIID and to elucidate the roles of TAF(II)s in gene activation, we have cloned the mouse TAF(II)55 subunit of TFIID and further isolated mouse TFIID from a murine FM3A-derived cell line that constitutively expresses FLAG-tagged mouse TAF(II)55. Both mouse and human TFIIDs are capable of mediating transcriptional activation by Gal4 fusions containing different activation domains in a highly purified human cell-free transcription system devoid of TFIIA and Mediator. Although TAF(II)-independent activation by Gal4-VP16 can also be observed in this highly purified human transcription system with either mouse or yeast TBP, TAF(II)s are strictly required for estrogen receptor-mediated activation independently of the core promoter sequence. In addition, TAF(II)s are necessary for transcription from a preassembled chromatin template. These findings clearly demonstrate an essential role of TAF(II)s as a transcriptional coactivator for estrogen receptor and in chromatin transcription.

Animals↗
PubMed1989

Macrophage-mediated islet cell cytotoxicity in BB rats.

Islet cell killing mediated by natural killer cells and T-lymphocytes in diabetes-prone (DP) and diabetic BB rats has been described, but other killing mechanisms may also be involved. Histopathologic studies suggest that macrophages are the first immune cells to infiltrate islets. To determine if macrophages are the first cells mediating islet damage, macrophage-mediated cytotoxicity was evaluated in BB rats of different ages. Splenic macrophages isolated from DP rats at 33, 100, 120, and 140 days of age showed no enhanced islet killing compared with diabetes-resistant rats. Killing at diabetes onset (121 +/- 14 days) was markedly increased (43 +/- 9.3%) compared with age-matched diabetes-resistant controls (19 +/- 8.3%, P less than .001). Islet inflammation was monitored at all time points. At 120 and 140 days of age, 9 of 11 (82%) DP rats had insulitis, and cytotoxicity was increased in 6 of 11 (55%) rats, which is similar to the number of DP rats that progress to diabetes. At 100 days, 3 of 6 (50%) DP rats again showed diabetic levels of killing, even in the absence of insulitis. These data indicate that 1) islet inflammation is dissociated from clinical diabetes onset, 2) splenic macrophages may have islet-killing potential before islet inflammation, 3) macrophage-mediated islet killing is elevated in all animals immediately after diabetes onset, and 4) macrophages, in addition to natural killer cells and T-lymphocytes, are responsible for cell-mediated islet destruction and thus are candidates for the first cellular effector to result in islet killing.

Aging↗
PubMed1982

Effects of adrenalectomy and glucocorticosteroid therapy on bone marrow T cells. Effect on T cell traffic and graft-versus-host (GVH) reactivity.

The effects of bilateral adrenalectomy (Ax) and glucocorticosteroid (GCS) treatment on the migratory behavior of circulating T cells in mice were evaluated by a 51Cr lymphocyte migration assay and two graft-versus-host (GVH) assays. The major new findings were that bilaterally adrenalectomizing a mouse effects it in two interrelated ways: 1) It decreases the accumulation of adoptively transferred 51Cr-labeled T cells to the bone marrow; and 2) it reduces the GVH reactivity of bone marrow cells. We also confirmed previous studies showing increases in the accumulation of T cells and increases in T cell-mediated GVH reactivity in the marrow of GCS-treated mice. We conclude that Ax has an opposite effect to that of GCS treatment on the intramarrow traffic of T cells and on T cell-mediated GVH reactivity of marrow cells.

Adrenalectomy↗
PubMed1978

Antiserum to surface antigens as a marker for cultured rat lung endothelial cells (1).

Antibodies were developed in rabbits against an established line of endothelial cells from normal adult rat lung. Pre- and postimmunization sera were tested for antibody activity by the indirect immunofluorescence technique. Preimmunization serum failed to react with the endothelial cells, whereas the antibody titer of postimmunization serum from two rabbits was 1:512. Organ specificity and species specificity were assessed by absorbing the serum with packed dissociated cells from different organs of the rat and lung cells of other species. Only cells obtained from rat lung absorbed the antibodies completely. The antiserum showed some crossreactivity with the other cultured cells but the pattern of fluorescence was different. In the presence of complement the antiserum was found to be cytotoxic to cultured rat lung endothelial cells but not to the other crossreacting cells.

Animals↗
PubMed1972

Cell-mediated tumor allograft immunity: in vitro transfer with RNA.

Specific inhibition of migration of spleen cells from C57B1/6J mice, which had rejected A/J sarcoma-1 tumors, occurred in the presence of A/J lymph mode antigens. The migration inhibitory effect was transferable to normal C57B1/6J spleen cells by RNA extracted from lymph nodes and spleens of immunized animals.

Animals↗