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[[Neural crest]] cells are a group of temporary, [[Cell potency#Multipotency|multipotent]] (can give rise to some other types of cells but not all) cells that are pinched off during the formation of the [[neural tube]] (precursor to the [[spinal cord]] and brain) and therefore are found at the dorsal (top) region of the neural tube during development.<ref name="Kirby (1987)">{{Cite journal |last=Kirby |first=Margaret L |year=1987 |title=Cardiac Morphogenesis—Recent Research Advances |url=https://www.nature.com/articles/pr198744.pdf |journal=Pediatric Research |publisher=Springer Science and Business Media LLC |volume=21 |issue=3 |pages=219–224 |doi=10.1203/00006450-198703000-00001 |pmid=3562119 |issn=0031-3998 |doi-access=free}}</ref> They are derived from the [[ectoderm]] germ layer, but are sometimes called the fourth germ layer because they are so important and give rise to so many other types of cells.<ref name="Kirby (1987)" /><ref name="Gilbert (2010)">{{Cite book |last=Gilbert |first=S. F. |title=Developmental biology |publisher=Sinauer Associates |year=2010 |isbn=978-0-87893-243-6 |edition=6th |___location=Massachusetts |pages=373–389 |chapter=The Neural Crest |chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK10065/}}</ref> They migrate throughout the body and create a large number of differentiated cells such as [[neuron]]s, glial cells, pigment-containing cells in skin, skeletal tissue cells in the head, and many more.<ref name="Kirby (1987)" /><ref name="Gilbert (2010)" />
Cardiac neural crest cells (CNCCs) are a type of neural crest cells that migrate to the circumpharyngeal ridge (an arc-shape ridge above the [[pharyngeal arch]]es) and then into the 3rd, 4th and 6th pharyngeal arches and the cardiac outflow tract (OFT).<ref name="Kirby (1987)" /><ref name="Gilbert (2010)" /><ref name="Kuratani (1992)">{{Cite journal |last1=Kuratani |first1=Shigeru C. |last2=Kirby |first2=Margaret L. |date=1992 |title=Migration and distribution of circumpharyngeal crest cells in the chick embryo |url=https://onlinelibrary.wiley.com/doi/10.1002/ar.1092340213 |journal=The Anatomical Record |volume=234 |issue=2 |pages=263–280 |doi=10.1002/ar.1092340213 |issn=0003-276X |pmid=1384396|url-access=subscription }}</ref>
They extend from the [[otic placode]]s (the structure in developing embryos that will later form the ears) to the third [[somite]]s (clusters of [[mesoderm]] that will become skeletal muscle, vertebrae and dermis).<ref name="Kirby (1987)" /><ref name="Gilbert (2010)" />
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=== Wnt ===
Wnt proteins are extracellular [[growth factor]]s that activate intracellular signalling pathways. There are two types of pathways: canonical and non-canonical. The classic canonical Wnt pathway involves [[β-catenin]] protein as a signaling mediator. Wnt maintains β-catenin by preventing against [[Proteasome]] degradation. Thus, β-catenin is stabilized in the presence of Wnt and regulates gene transcription through interaction with TCF/LEF transcription factors.<ref name="Gessert (2010)">{{Cite journal |last1=Gessert |first1=Susanne |last2=Kühl |first2=Michael |date=2010-07-23 |title=The Multiple Phases and Faces of Wnt Signaling During Cardiac Differentiation and Development |url=https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.110.221531 |journal=Circulation Research |volume=107 |issue=2 |pages=186–199 |doi=10.1161/CIRCRESAHA.110.221531 |pmid=20651295 |issn=0009-7330|url-access=subscription }}</ref> The canonical Wnt/β-catenin pathway is important for control of cell proliferation.<ref name="Kirby (2010)2">{{Cite journal |last1=Kirby |first1=Margaret L. |last2=Hutson |first2=Mary R. |date=2010 |title=Factors controlling cardiac neural crest cell migration |journal=Cell Adhesion & Migration |volume=4 |issue=4 |pages=609–621 |doi=10.4161/cam.4.4.13489 |issn=1933-6918 |pmc=3011257 |pmid=20890117 |doi-access=free}}</ref> The non-canonical Wnt pathway is independent of β-catenin and has an inhibitory effect on canonical Wnt signaling.<ref name="Gessert (2010)" />
Wnt signaling pathways play a role in CNCC development as well as OFT development.<ref name="Gessert (2010)" /> In mice, decrease of β-catenin results in a decrease in the proliferation of CNCCs.<ref name="Gessert (2010)" /> Downregulation of the Wnt coreceptor [[Lrp6]] leads to a reduction of CNCCs in the dorsal neural tube and in the pharyngeal arches, and results in ventricular, septal, and OFT defects.<ref name="Gessert (2010)" /> Canonical Wnt signaling is especially important for cell cycle regulation of CNCC development and the initiation of CNCC migration.<ref name="Gessert (2010)" /> Non-canonical Wnt signaling plays a greater role in promoting cardiac differentiation and OFT development.<ref name="Gessert (2010)" />
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=== Bone morphogenetic proteins ===
[[Bone morphogenetic protein]]s (BMPs) are required for neural crest cell migration into the cardiac cushions (precursors to heart valves and septa) and for differentiation of neural crest cells to smooth muscle cells of the aortic arch arteries. In neural crest–specific Alk2-deficient embryos, the cardiac cushions of the outflow tract are deficient in cells because of defects in neural crest cell migration.<ref name="Kaartinen (2004)">{{Cite journal |last1=Kaartinen |first1=Vesa |last2=Dudas |first2=Marek |last3=Nagy |first3=Andre |last4=Sridurongrit |first4=Somyoth |last5=Lu |first5=Min Min |last6=Epstein |first6=Jonathan A. |date=2004-07-15 |title=Cardiac outflow tract defects in mice lacking ALK2 in neural crest cells |url=https://journals.biologists.com/dev/article/131/14/3481/52362/Cardiac-outflow-tract-defects-in-mice-lacking-ALK2 |journal=Development |volume=131 |issue=14 |pages=3481–3490 |doi=10.1242/dev.01214 |issn=1477-9129 |pmid=15226263|url-access=subscription }}</ref>
=== Fibroblast growth factor 8 ===
[[Fibroblast growth factor 8]] (FGF8) transcription factors are essential for regulating the addition of secondary heart field cells into the cardiac outflow tract. FGF8 mouse mutants have a range of cardiac defects including underdeveloped arch arteries and transposition of the great arteries.<ref name="Abu-Issa (2002)">{{Cite journal |last1=Abu-Issa |first1=Radwan |last2=Smyth |first2=Graham |last3=Smoak |first3=Ida |last4=Yamamura |first4=Ken-ichi |last5=Meyers |first5=Erik N. |date=2002-10-01 |title=Fgf8 is required for pharyngeal arch and cardiovascular development in the mouse |url=https://journals.biologists.com/dev/article/129/19/4613/20179/Fgf8-is-required-for-pharyngeal-arch-and |journal=Development |volume=129 |issue=19 |pages=4613–4625 |doi=10.1242/dev.129.19.4613 |pmid=12223417 |issn=1477-9129|url-access=subscription }}</ref><ref name="Frank (2002)">{{Cite journal |last1=Frank |first1=Deborah U. |last2=Fotheringham |first2=Lori K. |last3=Brewer |first3=Judson A. |last4=Muglia |first4=Louis J. |last5=Tristani-Firouzi |first5=Martin |last6=Capecchi |first6=Mario R. |last7=Moon |first7=Anne M. |date=2002-10-01 |title=An <i>Fgf8</i> mouse mutant phenocopies human 22q11 deletion syndrome |journal=Development |publisher=The Company of Biologists |volume=129 |issue=19 |pages=4591–4603 |doi=10.1242/dev.129.19.4591 |issn=1477-9129 |pmc=1876665 |pmid=12223415 |doi-access=free}}</ref>
=== GATA ===
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