anchor.diff:                              <div class="inner">
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                            			<p>
  -                         				Striatins  act  as  both  calciumdependent  signaling  proteins  and  scaffolding 
  -										proteins,  linking  calciumsensing  signaling  events  with  cellular  action  [1]. Strn3
  +                         				Striatins  act  as  both  calcium-dependent  signaling  proteins  and  scaffolding 
  +										proteins,  linking  calcium-sensing  signaling  events  with  cellular  action  [1]. Strn3
   										homozygous  mutants  show  complete  preweaning  lethality,  with  embryonic 
   										lethality  occurring  around  E15.5.  Surviving  embryos  are  smaller  in  size  and 
   										display  both  hemorrhaging  and  severe  edema  (Fig  1,  left  panels).  MicroCT 
   										analyses reveal small, but consistent septal defects in heart (Fig 1, right panels).  Multiple  phenotypes  are  observed  in  heterozygous  adult  animals,  including 
   										abnormal  blood  chemistry  and  hematology,  impaired  glucose  tolerance  and 
  -										abnormal  behavior,  among  others.  A  Genomewide  association  study  linking 
  +										abnormal  behavior,  among  others.  A  Genome-wide  association  study  linking 
   										Strn3 with the canine disease Arrhythmogenic Right Ventricular Cardiomyopathy 
   										(ARVC) supports a role in cardiac function [2].  
   									</p>
  
positive.code: 										Homozygous mutants show complete preweaning lethality, with embryonic lethality occurring after 										
  										E18.5. Hemorrhaging is seen in surviving E18.5 mutants, as is severe edema and small embryo size 										
  										(Fig 1, left). Among other defects, microCT analysis 	reveals brain defects, lung hypoplasia and absent										
  										renal pelvis in the kidney (Fig 2, right). Phenotypes of heterozygotes include abnormal body composition										
  										and abnormal blood chemistry.
  									</p>
                          			
  
negative.code:                             	<div class="half">
                           			<p>
                           				Rab34 is a member of the RAS oncogene family, which are small GTPases
  										involved in intracellular vesicle transport. Rab34 is known to be Golgi-bound, involved in lysosomal positioning. 
  										Rab34 is a potential target of Gli1 and a possible 
  										component of hedgehog signaling. The Rab34 knockout is the first reported null allele for this gene, 
  										resulting in complete preweaning lethality.  Phenotypes 
  										include patterning defects, such as polydactyly and facial clefting, as well as abnormal eye 
  										development and severe lung hypoplasia (Fig  1,  lu = lung). The mutants are 
  										subviable at E18.5, lethality presumably occurring perinatally.
  									</p>
  									                        			
  