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SIL3 ... likelyto influenceauxin homeostasis
stress hormones or other hormones(passive) triggered byendolymphatic homeostasis
inflammation , oxidative stress , mitochondrial dysfunction and proapoptotic / antiapoptotic dysregulation(passive) caused byPerturbed homeostasis
An age - related breakdown in the mechanisms controllingcould contributeCa2+]i homeostasis
an uncontrolled rise in heat production(passive) caused bythermoregulatory homeostasis
inflammation responsecan influenceimmunological homeostasis
genesinfluencingauxin homeostasis
activation of olfactory receptor signaling by external compoundscan influencemelanocyte homeostasis
defects in ion channels(passive) caused byCa2+]cyt homeostasis
by which Cd stressinfluencesauxin homeostasis
mitochondrial FtSH4 gene - mediated peroxidase accumulation(passive) caused byauxin homeostasis
to less chest tightness , cough , shortness of breath , and wheezingledto less chest tightness , cough , shortness of breath , and wheezing
to increased stress resistanceleadingto increased stress resistance
the development of inflammatory processespreventsthe development of inflammatory processes
to cell damage and further deathleadingto cell damage and further death
to peripheral neuropathy ( 21contributesto peripheral neuropathy ( 21
to improved LV functionleadingto improved LV function
to the toxicity of nitric oxide in cultured hippocampal neuronscontributesto the toxicity of nitric oxide in cultured hippocampal neurons
potentiallyinfluencepotentially
in increased [ Ca2+]i , such as inhibition of PKA or PKC during stimulationresultin increased [ Ca2+]i , such as inhibition of PKA or PKC during stimulation
to the development and progression of the disorderleadingto the development and progression of the disorder
in [ Ca2+]i increases that reach ≥250 nM , such as in vivo cochlea removal or mGluR antagonism with MCPGresultin [ Ca2+]i increases that reach ≥250 nM , such as in vivo cochlea removal or mGluR antagonism with MCPG