Associated Papers
Novel Insights into the Enigmatic Genetics of Male Breast Cancer in China.
Lang GT et al.
Pathophysiology : the Official Journal of the International Society for Pathophysiology, 2026
41718387 (PubMed )
Supplement: pathophysiology-33-00009-s001.zip › Supplementary_Table_1.pdf
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
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
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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