Associated Papers
Three regulatory elements upstream of LMO4 are strongly associated with intermittent fertilization intensity in Chicken.
Wang L et al.
Poultry Science, 2025
The role of SLC26A8 homozygous variants in male infertility and flagellum abnormalities.
Mao B et al.
Asian Journal of Andrology, 2024
Detection of germline variants with pathogenic potential in 48 patients with familial colorectal cancer by using whole exome sequencing.
Singh AK et al.
Bmc Medical Genomics, 2023
37296477 (PubMed )
Supplement: 12920_2023_1562_MOESM3_ESM.xlsx › Stage2-Class4-5_variants
The heterozygous mutations of SLC26A8 are not the main actors for male infertility.
Liu M et al.
Human Mutation, 2022
Novel biallelic mutations in SLC26A8 cause severe asthenozoospermia in humans owing to midpiece defects: Insights into a putative dominant genetic disease.
Gao Y et al.
Human Mutation, 2022
Neurodegenerative VPS41 variants inhibit HOPS function and mTORC1-dependent TFEB/TFE3 regulation.
van der Welle REN et al.
Embo Molecular Medicine, 2021
33851776 (PubMed )
Supplement: EMMM-13-e13258-s002.zip › Dataset_EV1.xlsx › Sheet1
Molecular analysis of human solute carrier SLC26 anion transporter disease-causing mutations using 3-dimensional homology modeling.
Rapp C et al.
Biochimica Et Biophysica Acta. Biomembranes, 2017
Functional interaction of the cystic fibrosis transmembrane conductance regulator with members of the SLC26 family of anion transporters (SLC26A8 and SLC26A9): physiological and pathophysiological relevance.
El Khouri E et al.
The International Journal of Biochemistry & Cell Biology, 2014
N-glycosylation and topology of the human SLC26 family of anion transport membrane proteins.
Li J et al.
American Journal of Physiology. Cell Physiology, 2014
Missense mutations in SLC26A8, encoding a sperm-specific activator of CFTR, are associated with human asthenozoospermia.
Dirami T et al.
American Journal of Human Genetics, 2013
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