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Kell blood group, metallo-endopeptidase

This gene encodes a type II transmembrane glycoprotein that is the highly polymorphic Kell blood group antigen. The Kell glycoprotein links via a single disulfide bond to the XK membrane protein that carries the Kx antigen. The encoded protein contains sequence and structural similarity to members of the neprilysin (M13) family of zinc endopeptidases. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ACID, CAN, POLYMERASE, CD45, HAD
Papers on Kel
Riboflavin-ultraviolet light pathogen reduction treatment does not impact the immunogenicity of murine red blood cells.
Hendrickson et al., United States. In Transfusion, Jan 2016
STUDY DESIGN AND METHODS: Transgenic mice expressing a model (HOD) antigen, authentic human (hGPA or KEL) antigens, or natural fluorescence (uGFP) on their RBCs were utilized as blood donors.
TMEM175 Is an Organelle K(+) Channel Regulating Lysosomal Function.
Ren et al., Philadelphia, United States. In Cell, Sep 2015
Here, we directly recorded organelle K(+) conductance and discovered a major K(+)-selective channel KEL on endosomes and lysosomes.
The insulator protein Suppressor of Hairy wing is required for proper ring canal development during oogenesis in Drosophila.
Labrador et al., Knoxville, United States. In Dev Biol, Aug 2015
Fluorescence microscopy reveals that lack of Su(Hw) leads to excess accumulation of Kelch (Kel) and Filament-actin (F-actin) proteins in the ring canal structures of developing egg chambers.
Effect of diosmin on the intestinal absorption and pharmacokinetics of fexofenadine in rats.
Bedada et al., Warangal, India. In Pharmacol Rep, Apr 2015
In comparison with control, pretreatment with diosmin significantly increased peak plasma concentration (Cmax) and area under the concentration-time curve (AUC), while there was no significant change was observed in half life (T1/2), time to reach peak plasma concentration (Tmax) and elimination rate constant (Kel) of fexofenadine.
Evaluation of electrostatic binding of PAMAM dendrimers and charged phthalocyanines by fluorescence correlation spectroscopy.
Costa et al., Lisbon, Portugal. In Phys Chem Chem Phys, Mar 2015
The changes of binding affinity probed by varying the phthalocyanine charge, and by changing the ionic strength or pH conditions, allowed us to evaluate the electrostatic contribution (Kel) in dendrimer-phthalocyanine interactions.
Novel alleles at the Kell blood group locus that lead to Kell variant phenotype in the Dutch population.
de Haas et al., Amsterdam, Netherlands. In Transfusion, Feb 2015
BACKGROUND: Alloantibodies directed against antigens of the Kell blood group system are clinically significant.
454-Sequencing™ for the KEL, JR, and LAN Blood Groups.
Bugert et al., Mannheim, Germany. In Methods Mol Biol, 2014
The KEL (ISBT 006), JR (ISBT 032), and LAN (ISBT 033) blood group systems are defined by a complex genetics with a large number of exons, and numerous gene variants.
Three missense mutations found in the KEL gene lead to K(mod) or K0 red blood cell phenotypes.
Pierelli et al., Roma, Italy. In Transfusion, 2014
BACKGROUND: The KEL gene is highly polymorphic.
Semi-mechanistic modelling and simulation of inhibition of platelet aggregation by antiplatelet agents.
Kwon et al., Taejŏn, South Korea. In Basic Clin Pharmacol Toxicol, 2014
Time courses of plasma concentrations of the antiplatelet agents and their platelet aggregation effects were analysed using ADPAT V. Pharmacokinetic profiles were fitted to an extended parent-metabolite pharmacokinetic model, based on a two-compartment model, and the pharmacodynamic effects of the agents were fitted to a platelet aggregation effect model that consisted of the following parameters: Ks , the active-form platelet synthesis rate constant; K, the apparent reaction rate constant of the agent and active-form platelets; Kel-PRP , the apparent rate constant of platelets; and ε, an intrinsic activity parameter.
Three uncommon KEL alleles in one family with unusual Kell phenotypes explain a 35-year old conundrum.
Daniels et al., In Vox Sang, 2014
Molecular analysis of three uncommon KEL alleles elucidated the obscure pattern of inheritance of Kell antigens in one family.
Novel IVS6-13C>T mutation recognized as a cause of discrepancy between phenotyping and genotyping in KEL*3,4 polymorphism identification.
Bordin et al., In Transfusion, 2010
Novel IVS6-13C>T mutation recognized as a cause of discrepancy between phenotyping and genotyping in KEL*3,4 polymorphism identification.
Drosophila Kelch functions with Cullin-3 to organize the ring canal actin cytoskeleton.
Cooley et al., New Haven, United States. In J Cell Biol, 2010
demonstrate that association of Drosophila KEL with Cullin-3, likely in a cullin-RING ligase, is essential for the growth of Drosophila female germline ring canals.
Two novel null alleles of the KEL gene detected in two Chinese women with the K(null) phenotype.
Zhu et al., Shanghai, China. In Transfus Med, 2009
In screening 87665 unrelated healthy blood donors in China, two K(0) probands were detected; in exon 3, 185insT (Ser62Phe and a premature stop codon in exon 4
Changes in red cell ion transport, reduced intratumoral neovascularization, and some mild motor function abnormalities accompany targeted disruption of the Mouse Kell gene (Kel).
Lee et al., New York City, United States. In Am J Hematol, 2009
The targeted disruption of Kel in mouse enabled us to identify phenotypes that would not be easily detected in humans lacking Kell glycoprotein.
COP9 limits dendritic branching via Cullin3-dependent degradation of the actin-crosslinking BTB-domain protein Kelch.
Doronkin et al., Memphis, United States. In Plos One, 2008
COP9 limits dendritic branching via Cullin3-dependent degradation of the actin-crosslinking BTB-domain protein Kelch
[Immunohematologic characteristics in the Afro-caribbean population. Consequences for transfusion safety].
Noizat-Pirenne, Paris, France. In Transfus Clin Biol, 2003
Three levels of differences can be identified: common antigens in the RH, FY, JK and MNS blood groups, high frequency antigens in the RH, KEL, FY and MNS blood groups and low frequency antigens in the RH and KEL blood groups.
Insights into the structure and function of membrane polypeptides carrying blood group antigens.
Colin et al., Paris, France. In Vox Sang, 1997
This review will focus on selected blood groups systems (RH, JK, FY, LU, LW, KEL and XK) which are representative of these classes of molecules, in order to illustrate how these studies may bring new information on common and variant phenotypes and for understanding both the mechanisms of tissue specific expression and the potential function of these antigens, particularly those expressed in nonerythroid lineage.
Blood group polymorphisms: molecular approach and biological significance.
Daniels, Bristol, United Kingdom. In Transfus Clin Biol, 1997
Comparison of the position of these mutations within the KEL gene with clusters of antigens determined by an immunochemical technique, suggests that the Kell-system antigens are not linear and are probably discontinuous.
Molecular basis of Kell blood group phenotypes.
Lee, New York City, United States. In Vox Sang, 1996
The molecular basis of different Kell blood group phenotypes is reviewed.
[A molecular approach to the structure, polymorphism and function of blood groups].
Cartron, Paris, France. In Transfus Clin Biol, 1995
Most have been cloned and characterized recently, for instance MN antigens (glycophorin A), Ss antigens (glycophorin B), Gerbich antigens (glycophorins C and D) and antigens encoded by the RH, LW, KEL, FY, JK, XG, LU and XK loci.
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