Glynn, Rachel. : Rachel in the world : a memoir / Jane Bernstein
2007
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Glynn Research Institute. / http://id.loc.gov/authorities/names/n2002021874 : Wandering in the gardens of the mind : Peter Mitchell and the making of Glynn / John Prebble, Bruce Weber
A receptor subunit that is a shared component of the INTERLEUKIN-3 RECEPTOR; the INTERLEUKIN-5 RECEPTOR; and the GM-CSF RECEPTOR. High affinity receptor complexes are formed with each of these receptors when their respective alpha subunits are combined with this shared beta subunit
A receptor subunit that is a shared component of the INTERLEUKIN-3 RECEPTOR; the INTERLEUKIN-5 RECEPTOR; and the GM-CSF RECEPTOR. High affinity receptor complexes are formed with each of these receptors when their respective alpha subunits are combined with this shared beta subunit
A glycosphingolipid that accumulates due to a deficiency of hexosaminidase A or B (BETA-N-ACETYLHEXOSAMINIDASES), or GM2 activator protein, resulting in GANGLIOSIDOSES, heredity metabolic disorders that include TAY-SACHS DISEASE and SANDHOFF DISEASE
An autosomal recessive neurodegenerative disorder characterized by the onset in infancy of an exaggerated startle response, followed by paralysis, dementia, and blindness. It is caused by mutation in the alpha subunit of the HEXOSAMINIDASE A resulting in lipid-laden ganglion cells. It is also known as the B variant (with increased HEXOSAMINIDASE B but absence of hexosaminidase A) and is strongly associated with Ashkenazic Jewish ancestry
An autosomal recessive neurodegenerative disorder characterized by the onset in infancy of an exaggerated startle response, followed by paralysis, dementia, and blindness. It is caused by mutation in the alpha subunit of the HEXOSAMINIDASE A resulting in lipid-laden ganglion cells. It is also known as the B variant (with increased HEXOSAMINIDASE B but absence of hexosaminidase A) and is strongly associated with Ashkenazic Jewish ancestry
