Disease relevance of IGKV3D-15

• This report suggests that megadolichobasilar anomaly is potentially life-threatening, and that L16P is a disease-causing mutation in patients with Fabry's disease [1].
• The title compounds were evaluated against NSCLCN6 L16 bronchial epidermoid carcinoma in vitro and some of them were found to be active [2].

High impact information on IGKV3D-15

• When gas3/PMP22 point mutations (L16P, S79C, T118M, and G150D) are similarly overexpressed in NIH-3T3 cells, the induced apoptotic-like phenotype as compared to the wild-type is significantly reduced [3].
• Expression of IFN-stimulated response element- and gamma-activated sequence-controlled genes was severely impaired in cells infected with RV SAD L16 or in cells expressing RV P protein from transfected plasmids [4].
• By reverse genetics, we recovered viable RVs in which the strongly attenuating G/L gene border of wild-type (wt) RV (SAD L16) was replaced with N/P-derived gene borders (SAD T and SAD T2) [5].
• Peptides containing single glycine, serine, alanine, or threonine amino acid substitutions at the buried L9, L16, L23, and I26 hydrophobic core positions of a GCN4-based sequence were synthesized and studied by solution-phase and crystallographic techniques [6].
• The nucleotide sequences of resistant and susceptible isolates were compared, and a point mutation (thymine to guanine) that causes an Ile52-Ser substitution in ribosomal protein L16 was identified [7].

Biological context of IGKV3D-15

• Two large polypeptide fragments of ribosomal protein L16 were obtained by limited hydrolysis with trypsin and chymotrypsin [8].
• We also noted several discrepancies between phylogenetic trees based on 16S rRNA gene sequences and sequences of ribosomal proteins L16, L22 and S14, suggesting that horizontal gene transfer did play a significant role in the evolution of the S10-spc-alpha gene clusters [9].
• Genetic analysis disclosed a c.47T-->C missense mutation resulting in L16P in the amino acid sequence of the alpha-galactosidase protein [1].
• Assuming just one high affinity binding site on L16 for anionic lipid, the affinity of the site for di(C18 : 1)PS was calculated to be ca. 8 times that for di (C18 : 1)PC [10].

Anatomical context of IGKV3D-15

• The latter inhibitors act in substoichiometric concentration (KA = 0.32 X 10(6) M-1) and produce lasting ribosome damage due to a conformational alteration requiring proteins L7/L12, L8 and L16 [11].
• The binding to neutrophils of a monoclonal anti-LFA-1 antibody (NK1-L16) specific for an activation epitope of CD11a was increased a maximum of 28-fold and sixfold, respectively, after 1 and 5 min of preincubation with 10 nM LTB4 and fivefold after 5 min with PMA [12].

Associations of IGKV3D-15 with chemical compounds

• Experimental methods based on gas-phase chromatography were tested with a view to determine the gas-liquid n-hexadecane partition coefficients, log L16 of non-volatile compounds at 298.2 K [13].
• The single histidine in L16 appears to be important in the catalysis of peptide bond formation and transesterification [14].
• It was demonstrated that reliable values of log L16 of compounds more volatile than n-docosane can be obtained using either capillary, or packed columns [13].
• The sorption of VOCs as vapors to a typical organobentonite, modified with cetyltrimethylammonium bromide (CTMAB-bentonite), was characterized using a linear solvation energy relationship (LSER) of the type log Kc = c + rR2 + s pi2H + a sigma(alpha2)H + b sigma(beta2)H + l log L16 [15].
• The peptide Ac-KKGYL6WL8YKKA-amide (Y2L14) incorporated into bilayers of dinervonylphosphatidylcholine [di(C24 : 1)PC] whereas L16 did not incorporate into this lipid [10].

References