Disease relevance of CLEC10A

• A hereditary myopathy with lactic acidosis during physical exercise, low physical work capacity, and paroxysmal myoglobinuria (HML), called "Myopathy with deficiency of succinate dehydrogenase and aconitase" (McKusick 255125) has been described in 19 members of nine families who lived in two geographically separate areas in northern Sweden [1].
• Of the total of 74 HML-2 sequences, 18 corresponded to complete or near-complete proviruses, 49 were solitary long terminal repeats (LTRs), 6 were incomplete LTRs, and 1 was a SVA retrotransposon [2].
• We have studied the effects of plasma and of cumene hydroperoxide (CUM) on adenosine diphosphate ribosyl transferase (ADPRT) from mononuclear leukocytes (HML) of patients with colonic adenomatous polyps (n = 22), with colonic hyperplastic polyps (n = 5) and with neither type of polyp (controls) (n = 6) [3].
• To better define the relationship of these endogenous retroviruses, we identified ten new members of the HML-2 subgroup [4].
• Fab fragments of a murine monoclonal antibody against human osteosarcoma were labelled with radioiodinated 3'-iodohippuryl N-epsilon-maleoyl-L-lysine (HML) and were injected intravenously to tumour-bearing mice [5].

High impact information on CLEC10A

• To gain insight into the expansion of these elements in the genome during the course of primate evolution, we have identified 23 new members of the HERV-K (HML-2) group, which is thought to contain the most recently active members [6].
• The HML and HMR loci, which contain copies of the genes found at the yeast mating-type locus, are silenced, as are telomeres [7].
• 3'-[131I]Iodohippuryl N(epsilon)-maleoyl-L-lysine ([131I]HML) was conjugated with a thiolated Fab fragment because the glycyl-lysine sequence in HML is a substrate for a brush border enzyme and metaiodohippuric acid is released by cleavage of the linkage [8].
• HML/SE is a cytokine-dependent cell line established from childhood acute megakaryoblastic leukemia [9].
• Granulocyte-macrophage colony-stimulating factor or stem cell factor (SCF) alone could stimulate proliferation of HML/SE cells, however interleukin-3, interleukin-6, granulocyte colony-stimulating factor and thrombopoietin could not [9].

Biological context of CLEC10A

• At Least 50% of Human-Specific HERV-K (HML-2) Long Terminal Repeats Serve In Vivo as Active Promoters for Host Nonrepetitive DNA Transcription [10].
• In this study, we report the cloning of six full-length HML-2 RT genes, of which five contain an uninterrupted open reading frame [11].
• To investigate the utility of HML-2 polymorphisms as markers for the study of more recent human evolution, we compiled a list of the structure and integration sites of sequences that are unique to humans and screened each insertion for polymorphism within the human genome databases [2].
• Full-sized HERV-K (HML-2) human endogenous retroviral LTR sequences on human chromosome 21: map locations and evolutionary history [12].
• Hemagglutination inhibition assays suggest that HML binds GalNAc/Gal substituted with a neutral sugar through 1-3, 1-4, or 1-2 linkages in O-linked mucin-type glycans, and Fuc(alpha1-6)GlcNAc of N-linked glycoproteins [13].

Anatomical context of CLEC10A

• Glucocorticoid receptor binding in mononuclear leukocytes (HML) was characterized by homologous displacement of [3H]dexamethasone and compared with the dose-related inhibitory effect of dexamethasone on lysozyme synthesis [14].
• However, the most abundant expression was detected in lung (all subgroups), skeletal muscle (HML-4 and HML-5), placenta (HML-2 and HML-5), and kidney (HML-2, HML-3 and HML-5) [15].
• The dermal microenvironment induces the expression of the alternative activation marker CD301/mMGL in mononuclear phagocytes, independent of IL-4/IL-13 signaling [16].
• However, eosinophil-derived neurotoxin and eosinophil cationic protein were not detected or were only detected at a low level in the lysates of the HML cells treated with RA [17].

Associations of CLEC10A with chemical compounds

• Lysozyme activity from HML was not significantly affected by incubation with 1 mumol/L estradiol, progesterone, dehydroepiandrosterone, or aldosterone [14].
• Pretreatment of HML with vitamin E protected against these effects of CUM, while pretreatment with diamide (which depletes GSH) accentuated the effects [3].
• The use of HML as a radiolabelling reagent, combined with angiotensin II treatment, efficiently improved tumour targeting and enabled the imaging of tumours [5].
• In the present study we examined the effects of retinoic acid (RA) on the development of HML cells [17].

Regulatory relationships of CLEC10A

• Several proliferation inhibitors which removed the two-factor interaction on the growth of the HML-2 cells down-regulated the 145 kDa subunit of c-kit [18].

Analytical, diagnostic and therapeutic context of CLEC10A

• A calcium-type human macrophage lectin (HML) was prepared in a recombinant form, and its interaction with these glycopeptides was investigated by surface plasmon resonance (SPR) spectroscopy and fluorescence polarization [19].
• Southern blot analysis showed that some HML (human endogenous MMTV-like) subgroups (HML-4 and HML-5) were present in a few copies (about 5), whereas others (HML-1 to HML-3 and HML-6) were present in at least 10 to 20 copies per genome [15].
• This was monitored using HML group-specific oligonucleotide probes in hybridizations toward PCR amplificates of HML pol sequences and internal control [20].
• It was intended for calibration or performance testing of whole body counters and the HML subsequently built and tested that phantom [21].
• Preliminary N-terminal sequencing and biological assays strongly suggest that the HML may belong to a new class of algae lectins [22].

References