Disease relevance of CLEC4D

• Systemic lymphoma was present prior to, at presentation or at subsequent follow up in 26/68 (39%) of all lymphoma patients, 17% for MZL, 38% for DLBCL, 83% for FL, and 100% for MCL, CLL, PTCL and NKCL [1].

High impact information on CLEC4D

• CLECSF8 mRNA shows a monocyte/macrophage expression pattern [2].
• The CLECSF8 gene has been localized on the telomeric region of the NK gene complex on chromosome 12p13 close to MINCLE [2].
• Secondary outcomes were adrenal dysfunction, defined as an MPCL of <15 microg/dl, changes in cortisol levels over time, and mortality [3].
• The median MPCL was 15.75 microg/dl (interquartile range [IQR], 11.65 to 21.33 microg/dl) in 79 patients randomized to fluconazole and 16.71 microg/dl (IQR, 11.67 to 23.00 microg/dl) in 75 patients randomized to placebo (P = 0.52) [3].
• STUDY DESIGN AND METHODS: A calibration range of 0.083- to 2-percent D+ cells in the D-RBC mixtures (2-44 mL calculated FMH) was analyzed by use of a flow cytometer (XL-MCL, Coulter Electronics Ltd) [4].

Biological context of CLEC4D

• HECL, however, is most closely related to the sole group II C-type lectins reported to map near this region of the genome, the murine Nkcl and Mpcl genes [5].
• The genomic organization of the MCL gene and the sequence of the promoter region, with putative regulatory elements, were determined from a mouse MCL genomic DNA clone and are described here in detail [6].
• Based on these findings, it has been suggested that FH may function as a tumor suppressor gene in MCL [7].

Anatomical context of CLEC4D

• The longitudinal diameter of the attachment of ligaments was longer than the transverse one, except for the proximal attachment of the MCL [8].
• The objective of the present study was to compare the morphology of the lateral (LCL) and medial (MCL) collateral ligaments in human knees [8].

Associations of CLEC4D with chemical compounds

• After the determination of baseline Fluo-3 green fluorescence on a flow cytometer (EPICS XL-MCL, Coulter Electronics, Hialeah, FL), adequate agonists were added and time-dependent changes in Fluo-3 fluorescence were recorded on-line for up to 3 min [9].
• The activity of MCL was not inhibited by the presence of monosaccharides, such as Man, Fuc, Gal, Glc, GlcNAc, and NeuNAc [10].
• We evaluated the effects of formaldehyde and paraformaldehyde fixation on platelet P-selectin expression and fibrinogen binding using whole-blood flow cytometry and a Coulter EPICS XL-MCL cytometer [11].
• MCL activity was also inhibited by N-acetyl-d-galactosamine, human embryonic alpha-1-acid glycoprotein, and highly branched mannans from marine halophilic bacteria [10].
• All these results are consistent with the involvement of Trp residues in the sugar-binding activity of MCL [12].

Analytical, diagnostic and therapeutic context of CLEC4D

• SDS-PAGE showed that the MCL protein had a molecular mass of 138 kDa, and consisted of 74-, 34-, and 30-kDa subunits [10].
• Immunofluorescence staining revealed that MCL was bound to the surfaces of purified hypnospores from Perkinsus sp., which is a protozoan parasite of Manila clams [10].
• Affinity chromatography using mucin-Sepharose, ion-exchange chromatography with DEAE-Toyoperl, and gel filtration with Superose 6 were used for MCL isolation [10].

References