Endocrine Pancreas Development and Regeneration: Noncanonical Ideas From Neural Stem Cell Biology

Επιστημονική δημοσίευση - Άρθρο Περιοδικού uoadl:3169082 27 Αναγνώσεις

Μονάδα:
Ερευνητικό υλικό ΕΚΠΑ
Τίτλος:
Endocrine Pancreas Development and Regeneration: Noncanonical Ideas From
Neural Stem Cell Biology
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Loss of insulin-producing pancreatic islet beta-cells is a hallmark of
type 1 diabetes. Several experimental paradigms demonstrate that these
cells can, in principle, be regenerated from multiple endogenous sources
using signaling pathways that are also used during pancreas development.
A thorough understanding of these pathways will provide improved
opportunities for therapeutic intervention. It is now appreciated that
signaling pathways should not be seen as “on” or “off” but that
the degree of activity may result in wildly different cellular outcomes.
In addition to the degree of operation of a signaling pathway,
noncanonical branches also play important roles. Thus, a pathway, once
considered as “off” or “low” may actually be highly operational
but may be using noncanonical branches. Such branches are only now
revealing themselves as new tools to assay them are being generated. A
formidable source of noncanonical signal transduction concepts is neural
stem cells because these cells appear to have acquired unusual signaling
interpretations to allow them to maintain their unique dual properties
(self-renewal and multipotency). We discuss how such findings from the
neural field can provide a blueprint for the identification of new
molecular mechanisms regulating pancreatic biology, with a focus on
Notch, Hes/Hey, and hedgehog pathways.
Έτος δημοσίευσης:
2016
Συγγραφείς:
Masjkur, Jimmy
Poser, Steven W.
Nikolakopoulou, Polyxeni and
Chrousos, George
McKay, Ronald D.
Bornstein, Stefan R. and
Jones, Peter M.
Androutsellis-Theotokis, Andreas
Περιοδικό:
Nutrition and Diabetes
Εκδότης:
AMER DIABETES ASSOC
Τόμος:
65
Αριθμός / τεύχος:
2
Σελίδες:
314-330
Επίσημο URL (Εκδότης):
DOI:
10.2337/db15-1099
Το ψηφιακό υλικό του τεκμηρίου δεν είναι διαθέσιμο.