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10.1186/s40246-019-0233-3 http://scihub22266oqcxt.onion/10.1186/s40246-019-0233-3 31521203!6744627!31521203     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=31521203&cmd=llinks): Failed to open stream: HTTP request failed! 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SLC39A8 gene encoding a metal ion transporter: discovery and bench to bedside |pdf=|usr=}}{{31521203}} gab.com Text SLC39A8 gene encoding a metal ion transporter: discovery and bench to bedside JO: Hum Genomics http://www.kidney.de/pget.php?&tw=1&pmid=31521203 #FOAvip SLC39A8 is an evolutionarily highly conserved gene that encodes the ZIP8 metal cation transporter in all vertebrates. SLC39A8 is ubiquitously expressed, including pluripotent embryonic stem cells; SLC39A8 expression occurs in every cell type examined. Uptake of ZIP8-mediated Mn(2+), Zn(2+), Fe(2+), Se(4+), and Co(2+) represents endogenous functions-moving these cations into the cell. By way of mouse genetic differences, the phenotype of "subcutaneous cadmium-induced testicular necrosis" was assigned to the Cdm locus in the 1970s. This led to identification of the mouse Slc39a8 gene, its most closely related Slc39a14 gene, and creation of Slc39a8-overexpressing, Slc39a8(neo/neo) knockdown, and cell type-specific conditional knockout mouse lines; the Slc39a8(-/-) global knockout mouse is early-embryolethal. Slc39a8(neo/neo) hypomorphs die between gestational day 16.5 and postnatal day 1-exhibiting severe anemia, dysregulated hematopoiesis, hypoplastic spleen, dysorganogenesis, stunted growth, and hypomorphic limbs. Not surprisingly, genome-wide association studies subsequently revealed human SLC39A8-deficiency variants exhibiting striking pleiotropy-defects correlated with clinical disorders in virtually every organ, tissue, and cell-type: numerous developmental and congenital disorders, the immune system, cardiovascular system, kidney, lung, liver, coagulation system, central nervous system, musculoskeletal system, eye, and gastrointestinal tract. Traits with which SLC39A8-deficiency variants are currently associated include Mn(2+)-deficient hypoglycosylation; numerous birth defects; Leigh syndrome-like mitochondrial redox deficiency; decreased serum high-density lipoprotein-cholesterol levels; increased body mass index; greater risk of coronary artery disease, hypotension, cardiovascular death, allergy, ischemic stroke, schizophrenia, Parkinson disease, inflammatory bowel disease, Crohn disease, myopia, and adolescent idiopathic scoliosis; systemic lupus erythematosus with primary Sjogren syndrome; decreased height; and inadvertent participation in the inflammatory progression of osteoarthritis. Twit Text FOAVip SLC39A8 gene encoding a metal ion transporter: discovery and bench to bedside ????Hum Genomics http://www.kidney.de/pget.php?&tw=1&pmid=31521203 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31521203 #FOAvip English Wikipedia <ref>{{Cite pmid|31521203}}</ref> SLC39A8 gene encoding a metal ion transporter: discovery and bench to bedside #MMPMID31521203 Nebert DW; Liu Z Hum Genomics 2019[Sep]; 13 (Suppl 1): 51 PMID31521203show ga SLC39A8 is an evolutionarily highly conserved gene that encodes the ZIP8 metal cation transporter in all vertebrates. SLC39A8 is ubiquitously expressed, including pluripotent embryonic stem cells; SLC39A8 expression occurs in every cell type examined. Uptake of ZIP8-mediated Mn(2+), Zn(2+), Fe(2+), Se(4+), and Co(2+) represents endogenous functions-moving these cations into the cell. By way of mouse genetic differences, the phenotype of "subcutaneous cadmium-induced testicular necrosis" was assigned to the Cdm locus in the 1970s. This led to identification of the mouse Slc39a8 gene, its most closely related Slc39a14 gene, and creation of Slc39a8-overexpressing, Slc39a8(neo/neo) knockdown, and cell type-specific conditional knockout mouse lines; the Slc39a8(-/-) global knockout mouse is early-embryolethal. Slc39a8(neo/neo) hypomorphs die between gestational day 16.5 and postnatal day 1-exhibiting severe anemia, dysregulated hematopoiesis, hypoplastic spleen, dysorganogenesis, stunted growth, and hypomorphic limbs. Not surprisingly, genome-wide association studies subsequently revealed human SLC39A8-deficiency variants exhibiting striking pleiotropy-defects correlated with clinical disorders in virtually every organ, tissue, and cell-type: numerous developmental and congenital disorders, the immune system, cardiovascular system, kidney, lung, liver, coagulation system, central nervous system, musculoskeletal system, eye, and gastrointestinal tract. Traits with which SLC39A8-deficiency variants are currently associated include Mn(2+)-deficient hypoglycosylation; numerous birth defects; Leigh syndrome-like mitochondrial redox deficiency; decreased serum high-density lipoprotein-cholesterol levels; increased body mass index; greater risk of coronary artery disease, hypotension, cardiovascular death, allergy, ischemic stroke, schizophrenia, Parkinson disease, inflammatory bowel disease, Crohn disease, myopia, and adolescent idiopathic scoliosis; systemic lupus erythematosus with primary Sjogren syndrome; decreased height; and inadvertent participation in the inflammatory progression of osteoarthritis. |*Translational Research, Biomedical[MESH] |Animals[MESH] |Cation Transport Proteins/*genetics[MESH] |Evolution, Molecular[MESH] |Glycosylation[MESH] |Humans[MESH] |Ions[MESH] |Metals/*metabolism[MESH]SLC39A8 gene encoding a metal ion transporter: discovery and bench to (epmc).pdf DeepDyve Pubget Overpricing