D. On degradation by the proteasome. Matching: Match the human disease with the
ID: 260448 • Letter: D
Question
D. On degradation by the proteasome. Matching: Match the human disease with the defective: 7.9 gene that is i. ORAl1 A. X-linked agammaglobulinemia B. Wiscott-Aldrich ii. NEMO syndrome C. Severe combined ii. Btk immunodeficiency D. X-linked hypohidrotic iv. WASp ectodermal dysplasia and immunodeficiency 7.10 Fill-in-the-Blanks: Name the corresponding receptor or signaling component in its respective T/B cell counterpart: T cell CD3e:CD38:(CD3Y)2:(CD30)2 A. B. CD28 D. E. LAT:Gads:SLP-76 B cell CD21:CD19:CD81 C. Fyn, Blk, Lyn Syk F. General references. , B., Johnson A ?outie , peu u D-h--, K end Walter P. MolecularExplanation / Answer
7.9) A. X-linked agammaglobulinemia - iii. Btk.
XLA is caused by a mutation on the X chromosome of a single gene which produces an enzyme Bruton's tyrosine kinase or Btk.
B. Wiskott–Aldrich syndrome - iv. WASp.
Wiskott–Aldrich syndrome (WAS) is a rare X-linked recessive disease, which is characterized by eczema, thrombocytopenia, immune deficiency and bloody diarrhea. Their symptoms are produced by WAS mutations correlate with their effects on WASp.
C. Severe combined immunodeficiency - i. ORAl1.
Severe combined immunodeficiency is affected by severe bacterial, viral, or fungal infections.
D. X linked hypohidrotic ectodermal dysplasia and immunodeficiency - ii. NEMO.
They are uncommon genetic disorders, which result in abnormalities in ectodermally derived structures. The NEMO encoded by the IKBKG gene is unique in that mutations result in severe humoral and cellular immunologic defects.
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