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10.1038/s41598-021-87548-6 http://scihub22266oqcxt.onion/10.1038/s41598-021-87548-6 33859252!8050252!33859252     free     free     free Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2021 ; 11 (1): 8217 Nephropedia Template TP {{tp|p=33859252|t=2021. Cyclin M2 (CNNM2) knockout mice show mild hypomagnesaemia and developmental defects |pdf=|usr=}}{{33859252}} gab.com Text Cyclin M2 (CNNM2) knockout mice show mild hypomagnesaemia and developmental defects JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=33859252 #FOAvip Patients with mutations in Cyclin M2 (CNNM2) suffer from hypomagnesaemia, seizures, and intellectual disability. Although the molecular function of CNNM2 is under debate, the protein is considered essential for renal Mg(2+) reabsorption. Here, we used a Cnnm2 knock out mouse model, generated by CRISPR/Cas9 technology, to assess the role of CNNM2 in Mg(2+) homeostasis. Breeding Cnnm2(+/-) mice resulted in a Mendelian distribution at embryonic day 18. Nevertheless, only four Cnnm2(-/-) pups were born alive. The Cnnm2(-/-) pups had a significantly lower serum Mg(2+) concentration compared to wildtype littermates. Subsequently, adult Cnnm2(+/-) mice were fed with low, control, or high Mg(2+) diets for two weeks. Adult Cnnm2(+/-) mice showed mild hypomagnesaemia compared to Cnnm2(+/+) mice and increased serum Ca(2+) levels, independent of dietary Mg(2+) intake. Faecal analysis displayed increased Mg(2+) and Ca(2+) excretion in the Cnnm2(+/-) mice. Transcriptional profiling of Trpm6, Trpm7, and Slc41a1 in kidneys and colon did not reveal effects based on genotype. Microcomputed tomography analysis of the femurs demonstrated equal bone morphology and density. In conclusion, CNNM2 is vital for embryonic development and Mg(2+) homeostasis. Our data suggest a previously undescribed role of CNNM2 in the intestine, which may contribute to the Mg(2+) deficiency in mice and patients. Twit Text FOAVip Cyclin M2 (CNNM2) knockout mice show mild hypomagnesaemia and developmental defects ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=33859252 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33859252 #FOAvip English Wikipedia <ref>{{Cite pmid|33859252}}</ref> Cyclin M2 (CNNM2) knockout mice show mild hypomagnesaemia and developmental defects #MMPMID33859252 Franken GAC; Seker M; Bos C; Siemons LAH; van der Eerden BCJ; Christ A; Hoenderop JGJ; Bindels RJM; Muller D; Breiderhoff T; de Baaij JHF Sci Rep 2021[Apr]; 11 (1): 8217 PMID33859252show ga Patients with mutations in Cyclin M2 (CNNM2) suffer from hypomagnesaemia, seizures, and intellectual disability. Although the molecular function of CNNM2 is under debate, the protein is considered essential for renal Mg(2+) reabsorption. Here, we used a Cnnm2 knock out mouse model, generated by CRISPR/Cas9 technology, to assess the role of CNNM2 in Mg(2+) homeostasis. Breeding Cnnm2(+/-) mice resulted in a Mendelian distribution at embryonic day 18. Nevertheless, only four Cnnm2(-/-) pups were born alive. The Cnnm2(-/-) pups had a significantly lower serum Mg(2+) concentration compared to wildtype littermates. Subsequently, adult Cnnm2(+/-) mice were fed with low, control, or high Mg(2+) diets for two weeks. Adult Cnnm2(+/-) mice showed mild hypomagnesaemia compared to Cnnm2(+/+) mice and increased serum Ca(2+) levels, independent of dietary Mg(2+) intake. Faecal analysis displayed increased Mg(2+) and Ca(2+) excretion in the Cnnm2(+/-) mice. Transcriptional profiling of Trpm6, Trpm7, and Slc41a1 in kidneys and colon did not reveal effects based on genotype. Microcomputed tomography analysis of the femurs demonstrated equal bone morphology and density. In conclusion, CNNM2 is vital for embryonic development and Mg(2+) homeostasis. Our data suggest a previously undescribed role of CNNM2 in the intestine, which may contribute to the Mg(2+) deficiency in mice and patients. |Animals[MESH] |Animals, Newborn[MESH] |Cation Transport Proteins/*genetics[MESH] |Embryo, Mammalian[MESH] |Female[MESH] |Intellectual Disability/blood/complications/*genetics/pathology[MESH] |Magnesium Deficiency/blood/complications/*genetics/pathology[MESH] |Magnesium/blood[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Pregnancy[MESH]Cyclin M2 (CNNM2) knockout mice show mild hypomagnesaemia and developm(epmc).pdf DeepDyve Pubget Overpricing