Disease relevance of TRIM13

• RFP2, c13ORF1, and FAM10A4 are the most likely tumor suppressor gene candidates for B-cell chronic lymphocytic leukemia [1].
• Because homozygous deletions of chromosomal region 13q14.3 are found in a number of malignancies, including chronic lymphocytic leukemia (CLL) and multiple myeloma (MM), we suggest that RFP2 might be involved in tumor development [2].
• Conversely, a mutation in HIV-2 protease which changed Lys7 to Gln rendered the protein 3-fold less stable and shifted the position of the initial autoproteolytic cleavage from Phe3-Ser4 to Leu5-Trp6 [3].
• All cases showed antigenic profiles consistent with T-cell lymphoma, including expression of Leu-5 (CD2) antigen [4].
• A mutagenic approach to rendering autolytic cleavage sites less labile was applied to the primary cleavage site between Leu5 and Trp6 in human immunodeficiency virus-1 (HIV-1) protease [3].

High impact information on TRIM13

• Recloned secondary colonies of T cells reacted with Leu-5 and OKT-3 and were Ph' positive [5].
• With CFU-GEMMT colonies, T lymphocytes were identified by reaction with monoclonal antibodies Leu-5 and OKT-3; B cells were identified by reaction with B1 [5].
• From the minimally deleted region, 3 candidate genes have been isolated, RFP2, BCMS, and BCMSUN [6].
• The T cell LLs expressed Leu-1 in 100%, Leu-4 and Leu-9 in 95%, and Leu-5 in 85% of the cases [7].
• Distinctive changes in expression of Leu 1, Leu 2, and Leu 5 by the surface epithelial T-lymphocytes suggest that, although their total numbers are not increased, these cells are not passively crowded but have an active role, possibly as committed cytotoxic lymphocytes [8].

Biological context of TRIM13

• A "minimized" version of the RFP2 promoter could be used for overexpression of the various transgenes in the mammalian cells [9].
• We conclude that RFP2, c13ORF1, and a chromosome 13-specific ST13-like gene, FAM10A4, are the most likely candidates for such a type of B-CLL TSG [1].
• In addition, the RFP2/LEU5 transcript can be alternatively spliced to produce either several monocistronic transcripts or a putative bicistronic transcript encoding two separate open-reading frames, adding to the complexity of the locus [10].
• The dimerization domain was further defined by analyzing the ability of the N-terminal 13 amino acids or Leu-5, Phe-7, and Leu-9 deletion mutants of Fip-gts to interact with the wild type Fip-gts [11].
• In order to investigate the structure-activity relationship of [Leu5]- and [Met5]enkephalins, [(4'-bromo)Phe4, Leu5]-, [(4'-bromo)Phe4, Met5]- and [Met5] enkephalins were synthesized and crystallized [12].

Anatomical context of TRIM13

• Direct sequencing of the RFP2 gene revealed no mutations in six patients and four MM cell lines harboring deletions of the CDR [13].
• In a biopsy specimen from a lymph node, however, the malignant cells had a helper/inducer phenotype and also expressed the pan-T-cell antigens T11 and Leu-5 [14].
• These cells expressed pan-T cell antigens (Leu-4 and/or Leu-5) and helper T cell antigen (Leu-3) in each case [15].
• Leu5-beta h-endorphin was one-fifth as potent as beta h-endorphin in guinea pig ileum myenteric plexus, but was only slightly less active in mouse vas deferens and in guinea pig brain opiate receptor binding assay [16].
• Interaction of Leu5- and Met5-enkephalins with bilayer membranes of ditetradecylphosphatidylcholine results in a substantial refolding of the peptide backbones [17].

Associations of TRIM13 with chemical compounds

• These studies show that the mutation results in loss of a hydrogen bond between the 4-amino group of TMP and the carbonyl oxygen of Leu5 [18].
• The crystal structure of (Thr2, Leu5, d-Hiv8, Leu10)-cyclosporin (cyclic peptolide SDZ 214-103) has been determined as the unbound crystal form and as a complex with human cyclophilin A. This pair of structures provides an example of a significant difference in conformation between free and bound ligand in crystals [19].
• Phenylalanine in position 3 of bound peptides was shown to induce significant ring current shifts in several resonances assignable to the 1-8 sequence, including those of Leu-3 and/or Leu-5, but was without effect on Tyr-49 ring protons [20].
• [D-Ser2, Leu5, Thr6]enkephalin (DSLET) and [D-Ala2]deltorphin II, peptides selective for delta-opioid receptors, produced discriminative stimulus effects similar to DPDPE, and were approximately equipotent to DPDPE [21].
• Leu5-beta-endorphin and D-Leu5-beta-endorphin showed little or no release of Met-enkephalin [22].

Other interactions of TRIM13

• Distinct organization of the candidate tumor suppressor gene RFP2 in human and mouse: multiple mRNA isoforms in both species- and human-specific antisense transcript RFP2OS [2].
• Antigen-specific suppressor T lymphocytes in man make use of the same set of surface molecules as do cytolytic T lymphocytes: roles of Leu-2/T8, Leu-4/T3, Leu-5/T11, LFA-1 molecules [23].
• Since no single T-antigen, including Er and Er receptor (Leu-5), was expressed in all cases, a battery of monoclonal antibodies is necessary to detect PTL [24].
• However, a majority of cells (39-100%) reacted with OKT-11 (E-receptor) in 8 (44%) of 18 patients but with Leu-5 (E-receptors) in only 2 (22%) of 9 patients studied [25].

Analytical, diagnostic and therapeutic context of TRIM13

• Leu5/Met5-enkephalin immunoreactivity was separated by high-performance liquid chromatography into peaks composed of Leu5-enkephalin and Met5-enkephalin [26].
• Conversely, [D-Ala2, D-Leu5]enkephalin (DADLE) and [D-Ser2, Leu5] enkephalin-Thr6 (DSLET) showed decreased affinity to mu-ORs after treatment with anti-Gi2alpha IgGs, with no noticeable change following the use of IgGs to Gzalpha subunits [27].
• A three step immunoperoxidase technique on frozen sections was used to test a panel of 20 MoAb: anti-human Ig (heavy and light chains), To 15 (Pan B cells), Leu 1, T101, Leu 4, Leu 3a, Leu 5, OKT 8, OKT 6, Leu 7, anti-CALLA (IOT 5), Leu 10, anti-HLA-DR, OKM 1 and anti-dendritic reticulum cells (R 4/23) [28].
• The potencies of beta h-endorphin, Met (O)5-beta h-endorphin, and synthetic Leu5-beta h-endorphin have been compared in three bioassays of opioid activity, and in two radioimmunoassays [16].
• Renin was completely purified from human kidney cortex using a rapid 3-step procedure which included homogenization and ammonium sulfate precipitation, aminohexyl pepstatin affinity chromatography, and affinity chromatography using a synthetic octapeptide renin inhibitor (H-77) with a reduced peptide bond between Leu5 - Leu6 [29].

References