However, only data corresponding to the 12-week time point are reported because no deficiencies in grip strength due to genotype were detected prior to this age.
Supportively, DMD muscles are reported to have deficiencies in this protein [ 47, 48].
Hepatic copper levels below 3 6 μg/g ww are reported to indicate deficiency [ 3, 6].
Furthermore, patients with Mst1 deficiency are reported to have a primary immunodeficiency phenotype [ 8, 9].
Patients with MyD88 deficiency are reported to be susceptible to pyogenic bacterial infections including invasive pneumococcal disease.
It has been reported that deficiency in GDNF (Glial cell line-derived neurotrophic factor) level leads to a greater vulnerability to METH binge exposure in GDNF +/− mice [25].
Although no pathogenic MSH3 mutations have been reported, its deficiency is also suggested to cause low dinucleotide repeat instability.
It was reported that deficiency of CCR9, as well as CCR1, CCR2 and CCR5, did not attenuate a murine model of serum transfer arthritis [ 41].
Recently, it has been reported that deficiency in caspase-8 expression was a key determinant of apoptosis sensitivity of malignant brain tumours and melanoma (Fulda et al, 2001).
It has been reported that deficiency of FasL or Fas does not attenuate the inhibitory effect of PEDF on hypoxia-induced angiogenesis in OIR retinas [ 217].
