text: Yo, check it out, listen up, I got somethin' to say,
  'Bout them K(+)-Cl(-) cotransporters in a major way.
  KCC1 to KCC4, part of the SLC12 family,
  Electroneutral cation-coupled chloride cotransporters, can't you see?
  
  They move ions out the cell, regulate factors galore,
  Cell volume, chloride concentration, keepin' it hardcore.
  L-WNK1, a kinase all around,
  Gets activated by stress, chloride depletion, holdin' it down.
  
  It's linked to two syndromes, let me break it down,
  Pseudohypoaldosteronism type II, renal disease renowned.
  Hereditary sensory neuropathy 2, that's the neurological game,
  L-WNK1's involved, ain't that a shame?
  
  But its effect on KCC activity, we don't know,
  So we used Xenopus laevis oocytes, HEK-293 to show.
  When L-WNK1 was coexpressed, KCCs couldn't be activated,
  Cell swelling stopped 'em in their tracks, it's complicated.
  
  But hold up, wait a minute, there's a twist in the tale,
  NKCC1, the Na(+)-K(+)-2Cl(-) cotransporter, didn't fail.
  With L-WNK1 coexpression, it was remarkably increased,
  L-WNK1 got it jumpin', boostin' its beast.
  
  The negative effect on KCCs, it's all about the kinase,
  SPAK, OSR1, they're the ones we need to seize.
  If we eliminate the binding site, or the HQ motif,
  L-WNK1's impact on KCCs, we can relieve.
  
  So there you have it, L-WNK1's role is clear,
  Coordinately regulatin' NKCC1 and KCCs, no need to fear.
  Our data supports it, the interaction is key,
  L-WNK1 isoforms, keepin' the balance, you see.