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Here we generated Muc16 mutant mice using gene targeting in mouse embryonic stem (ES) cells.
We characterized the development of retinal vasculature in LRP5 mutant mice using specific retinal cell makers and a GFP transgene expressed in retinal endothelial cells.
We also accessed the size of adipocytes in wild type, Nscl-2, ob/ob, and Nscl-2 ×ob/ob compound mutant mice using flow cytometry.
Confirming a few previous studies that have reported PIT in C57BL/6J and (mixed or congenic) C57BL/6J-background mutant mice using comparable procedures as employed here [e.g.], [ 33], [34] [43], we found robust PIT in this strain.
We investigated adolescent mutant mice using a modified three-chamber social arena (Moy et al, 2004).
Finally, knock-out mutant mice, using a different construct, show craniofacial defects in addition to diaphragm malformations [ 12].
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Old studies on Edar mutant mice used either Edardl [1], [9] or Edarsleek [3] mice.
The Rev-Erbα−/−Per1Brdm1 double mutant mice used in this study were generated by crossing Rev-Erbα−/− [9] and Per1Brdm1 [20] single mutants.
Peritoneal macrophages from adult female C57BL/6J mice and all mutant mice used in this study were harvested three days after i.p. injection of concanavalin A [7].
The mutant mice used in this study carried the sirt1-null allele previously described [11] maintained on a mixed genetic background derived from intercrosses between the CD1 out bred strain and 129/J.
Furthermore, our results in males at E14.5 are comparable to those found by Lin et al. after they performed C57BL/6 backcrossing to the Dazl mutant mice used here [26], although the same group did not uncover similar defects in PGC number in Dazl null females [52].
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