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Figure 1.

Fri, 2021-07-09 17:21 -- admin
Summary: 
Intracellular fate of Z AAT. Under normal condition, AAT is mainly produced by hepatocytes and secreted into the bloodstream. Z AAT accumulates in the ER of the hepatocytes in the form of polymers leading to liver injury, whereas only a small proportion (∼15%) is secreted. The two major pathways involved in Z AAT degradation are: ubiquitin proteasome system and autophagy. Several transcription factors and environmental triggers induce SERPINA1 expression, affecting the burden of proteotoxic Z AAT. HNF: hepatocyte nuclear factors.
Type: 
Figure
Sub Component: 
Normal
Slug: 
F20
Highwire: Type: 
fragment
Highwire: Parent: 
Mechanisms of liver disease in AATD
HighWire: Journal/Corpus Code: 
ersbk
Highwire: pisa_id: 
ersbk;9781849841092/1/chapter_8/F20
Highwire: pisa_master: 
ersbk;9781849841092/1/chapter_8/F20
HighWire: Atom Path: 
/ersbk/9781849841092/9781849841092/SEC12/F20.atom
Highwire: cpath: 
/content/9781849841092/9781849841092/SEC12/F20
Image - Large: 
Large
Highwire: cpathalias: 
/content/ersbk/9781849841092/9781849841092/SEC12/F20
Image - Medium: 
Medium
Highwire: Variants: 
expansion
Image - Small: 
Small
Highwire: State: 
Released
Contributors: 
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<atom:contributor xmlns:atom="http://www.w3.org/2005/Atom" xmlns:hwp="http://schema.highwire.org/Journal" xmlns:nlm="http://schema.highwire.org/NLM/Journal" hwp:inherited="yes" nlm:contrib-type="author"><atom:name>Sergio Attanasio</atom:name><nlm:name name-style="western" hwp:sortable="Attanasio Sergio"><nlm:surname>Attanasio</nlm:surname><nlm:given-names>Sergio</nlm:given-names></nlm:name></atom:contributor>
<atom:contributor xmlns:atom="http://www.w3.org/2005/Atom" xmlns:hwp="http://schema.highwire.org/Journal" xmlns:nlm="http://schema.highwire.org/NLM/Journal" hwp:inherited="yes" nlm:contrib-type="author"><atom:name>Nicola Brunetti-Pierri</atom:name><atom:email>brunetti@tigem.it</atom:email><nlm:name name-style="western" hwp:sortable="Brunetti-Pierri Nicola"><nlm:surname>Brunetti-Pierri</nlm:surname><nlm:given-names>Nicola</nlm:given-names></nlm:name></atom:contributor>
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