Disease relevance of TMED8

• Using the monoclonal antibody L10 as a probe, sialophorin expression was detected on isolated T lymphocytes and thymocytes, B cell lines, monocytes, neutrophils, and platelets, but not on erythrocytes, fibroblasts, and glioblastoma cells [1].
• Two mAbs, BS1 and L10, stained 24 out of 31 (78%) nonhematopoietic tumors analyzed; ie., some tumors were positive for both antibodies, and others were positive for either L10 or BSL We have also found reactivity of these two anti-CD43 mAbs in 13 out of 20 metastases studied [2].
• Six monoclonal antibodies (M17, L1, L10, R10, I12, and K5) specific for gp95, a kD melanoma cell surface glycoprotein were also tested [3].
• Available sequences that correspond to the E. coli ribosomal proteins L11, L1, L10, and L12 from eubacteria, archaebacteria, and eukaryotes have been aligned [4].
• Moreover, reductions from baseline in all composite/individual daily reflective rhinitis symptom scores were significantly larger in patients receiving E20 than in patients receiving L10 or P [5].

High impact information on TMED8

• Treatment of monocytes with L10 mAb also caused dramatic increase in aggregation (homotypic adhesion) [6].
• Patients older than 50 years (group 2) received the chemotherapy arm composed of three monthly consolidation courses (DNR or ZRB, cytarabine, and asparaginase) followed by maintenance chemotherapy (modified L10 regimen) [7].
• In the present report we show that activation of both purified T lymphocytes and Jurkat cells, through CD43 cross-linking with the anti-CD43 L10 monoclonal antibody, induced CD43 association to Fyn kinase [8].
• Activation of mononuclear cells by L10 initiates phosphoinositides hydrolysis, C2+ mobilization, and protein kinase C (PKC) activation [9].
• The presence of manganese (Mn2+) significantly increases the binding of the platelet surface receptor GPIIb/IIIa to two synthetic peptides Gly-Arg-Gly-Asp-Ser-Pro (GRGDSP) and Leu-Gly-Gly-Ala-Lys-Gln-Ala-Gly-Asp-Val (L10) that contain the recognition sequences RGD and KQAGDV, respectively [10].

Chemical compound and disease context of TMED8

• During the past 14 years, 135 adults (greater than 15 years) with acute lymphoblastic leukemia (ALL) have been treated with one of three successive multidrug-intensive treatment protocols (L2, L10/10M, and L17/17M), each calling for 2.5 to 3 years of systemic chemotherapy and prophylactic intrathecal methotrexate without cranial irradiation [11].

Biological context of TMED8

• Treatment of PBMC and purified populations of T cells and monocytes with L10 induced the hydrolysis of phosphoinositides with the resultant generation of the phosphoinositide-derived second messengers diacylglycerol and inositol phosphates [12].
• Analysis of distribution of estimated haplotype frequencies revealed differences between suicide victims and control subjects, with an excess of haplotype L10 among suicide victims (p =.0112) [13].
• The factor binding site is located on the 50S ribosomal subunit and comprises proteins L7/12, L10, L11, the L11-binding region of 23S rRNA, and the sarcin-ricin loop of 23S rRNA [14].
• The frequencies of genotype combinations of the -800G/A, -509C/T, L10P, and R25P TGF-beta(1) polymorphisms were significantly different between the PDR and non-PDR groups (chi(2) = 37.83, df = 20, P < 10(-2)) [15].
• Allele frequencies of common TGF-beta1 polymorphisms (at positions -988C/A, -800G/A, -509C/T, +869T/C (L10P), and +915G/C (R25P)) were determined by PCR-based methodology [15].

Anatomical context of TMED8

• Recently, an anti-CD43 mAb (L10) was shown to induce proliferation in T cells comparable to that induced by anti-CD3 [16].
• The exchange of three large subunit proteins (L10, L19, L28) was detected by labeling of protein after ribosome synthesis had been inhibited with actinomycin D [17].
• L10 mAb inhibited the binding of 84-3C1 mAb to the cell membrane suggesting that both mAb recognized the same molecule [18].
• These results indicate that the ability of pathogenic Listeria to cause listeriosis is dependent on the nature of the food in which the pathogen is present, and that a traditional meat starter culture (FloraCarn) and some NTMS cultures, particularly L10, inhibit growth of the pathogen during passage through the gastrointestinal tract [19].
• We also produced MAb (L10) that detected IL-2 receptors (IL-2R) consistently expressed on in-vitro activated B cells as described above [20].

Associations of TMED8 with chemical compounds

• The connection of lipophilic gallic acid derivatives at the 5,5'- or 6,6'-positions of the rigid 2,6-bis(1-ethyl-benzimidazol-2-yl)pyridine core provides two pro-mesogenic tridentate ligands L10 and L12, whose molecular shapes, anisometries, and directional intermolecular pi-stacking can be tuned [21].
• Previous studies on T cell activation via CD43 antigen stimulation were limited to the use of L10, a monoclonal antibody (mAb) recognizing a sialic acid-independent epitope on the CD43 molecule [22].
• Four different Memorial Hospital protocols for systemic chemotherapy were used (LSA2L2 73%; L10 9%; L17 10%; L17M 8%); however, the IT (intrathecal) chemotherapy was uniform (Methotrexate: 6.0-6.25 mg/M2 per treatment course) and was included in the induction, consolidation, and maintenance phases of all treatment protocols [23].
• Although not apparent from crystallography, aromatic residues in L3, L5, L7, L8, and L10 affected FepA's interaction with FeEnt [24].
• The amino acid sequence of the rat 60S ribosomal subunit protein L10 was deduced from the sequence of nucleotides in two recombinant cDNAs and confirmed by determination of the NH2-terminal amino acid sequence in the protein [25].

Analytical, diagnostic and therapeutic context of TMED8

• We performed flow cytometry after immune staining using monoclonal antibodies to CD43 sialic acid-dependent (L60) and -independent (L10) epitopes [26].
• 3 polymorphisms located in the 5'region at positions -988 (C/A), -800 (G/A) and -509 (C/T) and 2 polymorphisms located at codons 10 (L10P) and 25 (R25P) of exon 1 were investigated by PCR methods [27].
• The overall, continuous sound in any bed space or patient care area shall not exceed: (1) an hourly Leq of 50 dB and (2) an hourly L10 of 55 dB, both A-weighted, slow response [28].
• RAPD-PCR using arbitrary primer L10 demonstrated intra-species homogeneity within PINLO strains with amplification profiles which differed from other Prevotella species tested [29].

References