Activation of the erythroid K-Cl cotransporter Kcc1 enhances sickle cell disease pathology in a humanized mouse model
Copyright policy )Activation of the erythroid K-Cl cotransporter Kcc1 enhances sickle cell disease pathology in a humanized mouse model
Key Points A missense mutation in the cytoplasmic tail of Kcc1 activates K-Cl cotransporter activity by impairing phosphorylation of nearby threonines. In vivo evidence shows that activation of Kcc1 directly contributes to the pathogenesis of sickle cell disease.
- Monash University Australia
- University of Adelaide Australia
- Alfred Health Australia
- University of Melbourne Australia
- Florey Institute of Neuroscience and Mental Health Australia
570, Mutation, Missense, 610, Anemia, Sickle Cell, Inbred C57BL, Mice, Animals, Humans, Inbred BALB C, Mice, Inbred BALB C, Symporters, Animal, Reverse Transcriptase Polymerase Chain Reaction, High-Throughput Nucleotide Sequencing, Anemia, Mice, Mutant Strains, Sickle Cell, Mutant Strains, Mice, Inbred C57BL, Disease Models, Animal, K Cl- Cotransporters, Disease Models, Mutation, Missense
570, Mutation, Missense, 610, Anemia, Sickle Cell, Inbred C57BL, Mice, Animals, Humans, Inbred BALB C, Mice, Inbred BALB C, Symporters, Animal, Reverse Transcriptase Polymerase Chain Reaction, High-Throughput Nucleotide Sequencing, Anemia, Mice, Mutant Strains, Sickle Cell, Mutant Strains, Mice, Inbred C57BL, Disease Models, Animal, K Cl- Cotransporters, Disease Models, Mutation, Missense
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