scholarly journals Growth arrest of PPP2R5C and PPP2R5D double knockout mice indicates a genetic interaction and conserved function for these PP2A B subunits

2021 ◽  
Author(s):  
Jade J. Dyson ◽  
Fatima Abbasi ◽  
Prajakta Varadkar ◽  
Brent McCright
Keyword(s):  
Knockout Mice ◽  
Genetic Interaction ◽  
Growth Arrest ◽  
Double Knockout ◽  
B Subunits

scholarly journals Exaggerated behavioral phenotypes in Fmr1/Fxr2 double knockout mice reveal a functional genetic interaction between Fragile X-related proteins

2006 ◽  
Vol 15 (12) ◽  
pp. 1984-1994 ◽  
Author(s):  
Corinne M. Spencer ◽  
Ekaterina Serysheva ◽  
Lisa A. Yuva-Paylor ◽  
Ben A. Oostra ◽  
David L. Nelson ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Genetic Interaction ◽  
Fragile X ◽  
Double Knockout ◽  
Behavioral Phenotypes ◽  
Related Proteins

scholarly journals Pkd1 and Wnt5a genetically interact to control lymphatic vascular morphogenesis in mice

2021 ◽  
Author(s):  
Tevin CY Chau ◽  
Sungmin Baek ◽  
Baptiste Coxam ◽  
Renae Skoczylas ◽  
Maria Rondon-Galeano ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Genetic Interaction ◽  
Lymphatic Vessels ◽  
Lymphatic Endothelial Cell ◽  
Wnt Signalling ◽  
Vascular Networks ◽  
Double Knockout ◽  
Vascular Morphogenesis ◽  
Vessel Networks ◽  
Canonical Wnt

Lymphatic vascular development is regulated by well-characterised signalling and transcriptional pathways. These pathways regulate lymphatic endothelial cell (LEC) migration, motility, polarity and and morphogenesis. Canonical and non-canonical WNT signalling pathways are known to control LEC polarity and development of lymphatic vessels and valves. PKD1, encoding Polycystin-1, is the most commonly mutated gene in polycystic kidney disease but has also been shown to be essential in lymphatic vascular morphogenesis. The mechanism by which Pkd1 acts during lymphangiogenesis remains unclear. Here we find that loss of non-canonical WNT signalling components Wnt5a and Ryk phenocopy lymphatic defects seen in Pkd1 knockout mice. To investigate genetic interaction, we generated Pkd1/Wnt5a double knockout mice. Loss of Wnt5a suppressed phenotypes seen in the lymphatic vasculature of Pkd1-/- mice and Pkd1 deletion suppressed phenotypes observed in Wnt5a-/- mice. Thus, we report mutually suppressive roles for Pkd1 and Wnt5a, with developing lymphatic networks restored to a more wild-type state in double mutant mice. This genetic interaction between Pkd1 and the non-canonical WNT signalling pathway ultimately controls LEC polarity and the morphogenesis of developing vessel networks. Our work suggests that Pkd1 acts at least in part by regulating non-canonical WNT signalling during the formation of lymphatic vascular networks.

3-Deazaadenosine Inhibits Vasa Vasorum Neovascularization in Aortas of ApoE-/-/LDL-/- Double Knockout Mice

2008 ◽  
Vol 180 (S 1) ◽  
Author(s):  
AC Langheinrich ◽  
D Sedding ◽  
M Kampschulte ◽  
J Wilhelm ◽  
W Haberbosch ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Vasa Vasorum ◽  
Double Knockout

scholarly journals Increase in SGLT1-mediated transport explains renal glucose reabsorption during genetic and pharmacological SGLT2 inhibition in euglycemia

2014 ◽  
Vol 306 (2) ◽  
pp. F188-F193 ◽  
Author(s):  
Timo Rieg ◽  
Takahiro Masuda ◽  
Maria Gerasimova ◽  
Eric Mayoux ◽  
Kenneth Platt ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Plasma Concentrations ◽  
Sglt2 Inhibitor ◽  
Double Knockout ◽  
Glucose Reabsorption ◽  
Urinary Glucose ◽  
Sglt2 Inhibition ◽  
Renal Glucose Reabsorption ◽  
Glucose Excretion ◽  
Free Plasma

In the kidney, the sodium-glucose cotransporters SGLT2 and SGLT1 are thought to account for >90 and ∼3% of fractional glucose reabsorption (FGR), respectively. However, euglycemic humans treated with an SGLT2 inhibitor maintain an FGR of 40–50%, mimicking values in Sglt2 knockout mice. Here, we show that oral gavage with a selective SGLT2 inhibitor (SGLT2-I) dose dependently increased urinary glucose excretion (UGE) in wild-type (WT) mice. The dose-response curve was shifted leftward and the maximum response doubled in Sglt1 knockout (Sglt1−/−) mice. Treatment in diet with the SGLT2-I for 3 wk maintained 1.5- to 2-fold higher urine glucose/creatinine ratios in Sglt1−/− vs. WT mice, associated with a temporarily greater reduction in blood glucose in Sglt1−/− vs. WT after 24 h (−33 vs. −11%). Subsequent inulin clearance studies under anesthesia revealed free plasma concentrations of the SGLT2-I (corresponding to early proximal concentration) close to the reported IC50 for SGLT2 in mice, which were associated with FGR of 64 ± 2% in WT and 17 ± 2% in Sglt1−/−. Additional intraperitoneal application of the SGLT2-I (maximum effective dose in metabolic cages) increased free plasma concentrations ∼10-fold and reduced FGR to 44 ± 3% in WT and to −1 ± 3% in Sglt1−/−. The absence of renal glucose reabsorption was confirmed in male and female Sglt1/Sglt2 double knockout mice. In conclusion, SGLT2 and SGLT1 account for renal glucose reabsorption in euglycemia, with 97 and 3% being reabsorbed by SGLT2 and SGLT1, respectively. When SGLT2 is fully inhibited by SGLT2-I, the increase in SGLT1-mediated glucose reabsorption explains why only 50–60% of filtered glucose is excreted.

P2.55 Mstn/Dysf double knockout mice gain muscle mass but no strength

2011 ◽  
Vol 21 (9-10) ◽  
pp. 676-677
Author(s):  
V. Schoewel ◽  
S. Adams ◽  
C. Herrmann ◽  
U. Zacharias ◽  
M. Boschmann ◽  
...  
Keyword(s):  
Muscle Mass ◽  
Knockout Mice ◽  
Double Knockout

scholarly journals Integrin α1/Akita double-knockout mice on a Balb/c background develop advanced features of human diabetic nephropathy

2012 ◽  
Vol 81 (11) ◽  
pp. 1086-1097 ◽  
Author(s):  
Ling Yu ◽  
Yan Su ◽  
Paisit Paueksakon ◽  
Huifang Cheng ◽  
Xiwu Chen ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Knockout Mice ◽  
Double Knockout
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