Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty-three dogs and cats with spontaneous tumors were treated with the immunostimulating polysaccharide acemannan by intraperitoneal and intralesional routes of administration. Tumors from 26 of these animals showed histopathological evidence of immunological attack as shown by marked necrosis or lymphocytic infiltration. Thirteen showed moderate to marked tumor necrosis or liquefaction. Twenty-one demonstrated lymphoid infiltration, and seven demonstrated encapsulation. Twelve animals showed obvious clinical improvement as assessed by tumor shrinkage, tumor necrosis, or prolonged survival; these included five of seven animals with fibrosarcomas. It is believed that acemannan exerts its antitumor activity through macrophage activation and the release of tumor necrosis factor, interleukin-1, and interferon.
Mol Biother 1991 Dec
PMID:Efficacy of acemannan in treatment of canine and feline spontaneous neoplasms. 176 73

Goat prothymosin alpha, a highly acidic polypeptide of pI3.5, 109 amino acid residues, has been isolated from lymphoid and non-lymphoid tissues of young female goats. Unlike rat, murine and porcine prothymosins alpha, goat prothymosin alpha appears at a higher concentration in the spleen compared with the thymus. The sequence of segments of the polypeptide involving known mutations has been determined, by automatic sequencing of its tryptic peptide fragments. The acidic amino acid-rich segment in the middle of the molecule, including residues 49-83, has not been sequenced. Goat prothymosin alpha closely resembles bovine prothymosin alpha, with only one substitution, proline for alanine at position 85. It also resembles human prothymosin alpha, with only three substitutions. It differs more significantly from rat and murine prothymosins alpha, by two deletions and three substitutions. The results show the highly conserved nature of the molecule, with substitutions at given positions only.
Mol Cell Biochem 1991 Nov 13
PMID:Isolation and partial sequence of goat spleen prothymosin alpha. 177 Sep 47

To understand the role of pituitary prolactin (PRL) and its receptor (PRL-R) in the growth and differentiation of lymphoid cells, PRL-R gene expression was analyzed in various lymphoid tissues and in a rat T lymphoma cell line, Nb2, which requires PRL for growth. The technique of reverse transcription coupled to polymerase chain reaction (RT-PCR) was used to detect the low abundance PRL-R transcripts. Within 30 min to 1 h, PRL stimulates a rapid but transient increase in PRL-R mRNA levels in Nb2 T cells. By 4 h, PRL-R mRNA returned to near basal levels and then gradually declined to a new steady-state level by 12 h. Significant increases in receptor RNA levels were observed in the presence of protein synthesis inhibitors, which suggests that PRL-R mRNA levels are under negative regulation. PRL-R gene expression was also demonstrated in normal mouse thymocytes, splenocytes, and in several lymphoid cell lines. The expression of the PRL-R gene in stimulated lymphoid cells provides additional evidence for the role of PRL as an immunomodulatory molecule.
Mol Cell Endocrinol 1991 Dec
PMID:Prolactin receptor gene expression in lymphoid cells. 179 4

The t(11;14)(q13;q32) translocation has been associated with human B-lymphocytic malignancy. Several examples of this translocation have been cloned, documenting that this abnormality joins the immunoglobulin heavy-chain gene to the bcl-1 locus on chromosome 11. However, the identification of the bcl-1 gene, a putative dominant oncogene, has been elusive. In this work, we have isolated genomic clones covering 120 kb of the bcl-1 locus. Probes from the region of an HpaII-tiny-fragment island identified a candidate bcl-1 gene. cDNAs representing the bcl-1 mRNA were cloned from three cell lines, two with the translocation. The deduced amino acid sequence from these clones showed bcl-1 to be a member of the cyclin gene family. In addition, our analysis of expression of bcl-1 in an extensive panel of human cell lines showed it to be widely expressed except in lymphoid or myeloid lineages. This observation may provide a molecular basis for distinct modes of cell cycle control in different mammalian tissues. Activation of the bcl-1 gene may be oncogenic by directly altering progression through the cell cycle.
Mol Cell Biol 1991 Oct
PMID:Characterization of a candidate bcl-1 gene. 183 29

The 78-kDa glucose-regulated protein (GRP78) is ubiquitously expressed in many cell types. Its promoter contains multiple protein-binding sites and functional elements. In this study we examined a high affinity protein-binding site spanning bp -198 to -180 of the rat grp78 promoter, using nuclear extracts from both B-lymphoid and HeLa cells. This region contains a sequence TGACGTGA which, with the exception of one base, is identical to the cAMP-response element (CRE). Site-directed mutagenesis reveals that this sequence functions as a major basal level regulatory element in hamster fibroblast cells and is also necessary to maintain high promoter activity under stress-induced conditions. By gel mobility shift analysis, we detect two specific protein complexes. The major specific complex I, while immunologically distinct from the 42-kDa CRE-binding protein (CREB), binds most strongly to the grp site, but also exhibits affinity for the CRE consensus sequence. As such, complex I may consist of other members of the CREB/activating transcription factor protein family. The minor specific complex II consists of CREB or a protein antigenically related to it. A nonspecific complex III consists of the Ku autoantigen, an abundant 70- to 80-kDa protein complex in HeLa nuclear extracts. By cotransfection experiments, we demonstrate that in F9 teratocarcinoma cells, the grp78 promoter can be transactivated by the phosphorylated CREB or when the CREB-transfected cells are treated with the calcium ionophore A23187. The differential regulation of the grp78 gene by cAMP in specific cell types and tissues is discussed.
Mol Endocrinol 1991 Dec
PMID:A binding site for the cyclic adenosine 3',5'-monophosphate-response element-binding protein as a regulatory element in the grp78 promoter. 183 91

BLAST-1 (CD48) (previously referred to as BCM-1 by the Human Gene Nomenclature Committee) is an early-activation-associated membrane glycoprotein expressed on the surface of human leukocytes and induced to a high level following infection of B cells by the Epstein-Barr virus. It is a member of the immunoglobulin superfamily, mediates cell adhesion, and has significant sequence homology to two other adhesion molecules, CD2 and LFA3. Here we report the isolation and characterization of the BLAST-1 gene. The gene is at least 28.6 kb in length, is split into 4 exons, and contains a restriction fragment-length polymorphism. The overall genomic organization is consistent with other members of the immunoglobulin superfamily, in which extracellular immunoglobulinlike domains are encoded by discrete exons. Transcription is initiated at a series of major and minor sites in both normal and tumor-derived lymphoid cells. Appropriately located TATA and CCAAT box sequences were not detected. These characteristics have also been demonstrated for the recently described B-cell-specific genes B29 and CD20. The expression of these genes in B cells may involve the use of multiple promoters and novel transcription initiator-binding proteins. A 1.58-kb genomic DNA fragment, consisting of the 5'-flanking region located immediately upstream of the ATG initiation codon, was able to drive the expression of a reporter gene in an orientation-dependent and tissue-restricted manner.
Mol Cell Biol 1991 Mar
PMID:Characterization of the Epstein-Barr virus-inducible gene encoding the human leukocyte adhesion and activation antigen BLAST-1 (CD48). 184 2

While it is known that the T-cell receptor beta chain gene is rearranged in fully developed murine thymic lymphomas induced by N-nitrosomethylurea and that the ras gene is activated in approximately 50% of these tumors (L. E. Diamond et al., Mol. Cell. Biol., 8: 2233-2236, 1988), it is unknown when these events occur or where the cells committed to a malignant phenotype are first located. We have studied these questions by treating mice with N-nitrosomethylurea, extracting thymocytes and bone marrow cells from the treated mice before they would have developed tumors, transferring the cells into recipient mice, monitoring those mice until they developed lymphoid tumors, and analyzing those tumors. This analysis showed that the initial cells committed to becoming malignant can be located in either the bone marrow or thymus and that both activation of the ras oncogene and rearrangements of the T-cell receptor gene can occur earlier than 30 days after N-nitrosomethylurea treatments. Furthermore, these results suggest that the T-cell receptor beta chain gene can undergo additional rearrangements during progression of a tumor.
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PMID:Staging of T-cell receptor beta chain gene rearrangements and ras oncogene mutations in the development of murine thymic lymphomas. 184 41

Mammalian hck, a member of the src family of tyrosine kinases, is expressed predominantly in cells of the myeloid and B-lymphoid lineages. Using mutational analysis, we have investigated the molecular basis of two immunoreactive forms of murine hck of 56 and 59 kDa found in numerous hemopoietic cell types. Our results indicate that translation of murine p59hck initiates from a CTG codon located 21 codons 5' of an ATG that is utilized to generate p56hck. We provide evidence that two human hck isoforms are generated by the same mechanism. Subcellular fractionation studies reveal that while p59hck and p56hck are associated with membranes of various murine B-lymphoid and myeloid cell lines, p59hck alone is also located in the cytosol. In contrast to membrane-associated p59hck, which is metabolically labeled with [3H]myristic acid and exhibits amphiphilic properties in Triton X-114 detergent, cytosolic p59hck is hydrophilic, suggesting that it is not acylated. Possible mechanisms are proposed to account for these observations.
Mol Cell Biol 1991 Sep
PMID:Two isoforms of murine hck, generated by utilization of alternative translational initiation codons, exhibit different patterns of subcellular localization. 187 27

Circulating lymphocytes are often used as a model for brain corticosteroid receptor regulation in clinical disease states, although it is not known if lymphoid receptors are regulated in a similar manner as brain receptors. In the present study the regulation of brain (hippocampus, frontal cortex, hypothalamus and striatum), lymphoid (circulating lymphocytes, spleen and thymus) and pituitary glucocorticoid receptors in response to alterations in circulating corticosterone levels was examined. Seven days following adrenalectomy, type II corticosteroid receptors (i.e. glucocorticoid receptors) were significantly increased in the hippocampus, frontal cortex and hypothalamus, but not in any other tissues. Administration of corticosterone (10 mg/kg) for 7 days significantly decreased type II as well as type I (i.e. mineralocorticoid receptors) receptors in the hippocampus. Type II receptors in the frontal cortex, circulating lymphocytes and spleen were also significantly decreased by chronic corticosterone treatment. Immobilization stress (2 h a day for 5 days) failed to alter receptor density in any of the tissues. These results demonstrate that homologous regulation of corticosteroid receptors by corticosterone does not invariably occur in all tissues and emphasize the complex degree of regulation of these receptors. However, the simultaneous downregulation of both hippocampal and lymphocyte glucocorticoid receptors by corticosterone provides support for the hypothesis that circulating lymphocytes do reflect some aspects of brain glucocorticoid receptor regulation.
J Steroid Biochem Mol Biol 1991 Aug
PMID:Corticosterone regulation of brain and lymphoid corticosteroid receptors. 188 73

The genes that encode the variable regions of immunoglobulin (Ig) heavy chains are encoded by three DNA segments: VH, D, and JH. During B-cell development these segments are brought together by a pair of site-specific DNA rearrangements. The first of these joins a D segment to a JH segment; the second brings a VH segment in apposition to a DJH unit. B-cell precursors that have undergone D-to-JH joining express transcripts that initiate at the 5' flanks of rearranged D segments (DJH transcription). In this study we have examined the coordination of D-to-JH rearrangement and DJH transcription. The B-lymphoid progenitor cell line HAFTL-1 cell clone, joining of distal D segments (DSP2 and DFL16) to JH is accompanied by an increase in the steady-state level of transcripts initiating 5' of the D coding region. Steady-state transcription of a DSP2 gene segment was undetectable prior to rearrangement and was observed to increase at least 20-fold upon joining to JH. In contrast, transcription from the 5' flank of DQ52, which lies within 700 bp of the JH cluster, was detected prior to rearrangement and did not increase significantly after rearrangement. The 5' flank of a DSP2 segment was found to support expression of a heterologous gene upon transfection into B progenitor cell lines. Expression from this DSP2 promoter was at least 30-fold higher in the presence of the Ig heavy-chain enhancer, in either orientation, than in its absence. A DNA fragment spanning the interval from -165 to +19 bp relative to the major DSP2 transcriptional start site retained enhancer-dependent promoter activity. These observations imply that activation of DSP12JH and DFL16JH transcription is coordinated with D-to-JH rearrangement by approximation of enhancer-dependent D promoter elements to the Ig heavy-chain enhancer. This interpretation is consistent with our observation that the DQ52 segment, which is closely linked to the JH cluster, is transcribed both before and after rearrangement.
Mol Cell Biol 1991 Apr
PMID:Coordination of immunoglobulin DJH transcription and D-to-JH rearrangement by promoter-enhancer approximation. 190 Sep 20


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