Publication for Ift88 and Dync2h1

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Ift88	intraflagellar transport 88	21821			[link]
mmu	Dync2h1	dynein cytoplasmic 2 heavy chain 1	110350

Pubmed ID	Priority	Text
21552265	0.98	Dync2h1lln/lln mutant MEFs, the amount of IFT88 in the cilium is increased and is found all along the axoneme.
	0.97	IFT88 (green, e) and Smo (green, f) and Gli2 (red, g) localize normally in primary cilia of MEFs derived from Dync2h1lln/lln Ift172avc1/+ embryos.
	0.96	IFT88 (green) accumulates specifically at the distal tips of both Ift122sopb/sopb and Dync2h1lln/lln Ift122sopb/sopb mutant MEF cilia.
	0.90	IFT88 (b, green), Smo (c, green) and Gli2 (d, green) in cilia (acetylated alpha-tubulin, red) appear normal in Dync2h1lln/lln Ift122sopb/+ mutants.
	0.87	IFT88 was enriched at cilia tips (Fig. 4c), as in Ift122sopb/sopb single mutants, and not accumulated along the cilium as seen in Dync2h1lln/lln cilia (Fig. 1c).
18488998	0.98	Ift88, Kif3a and Dync2h1) are required for activity of the mouse Hh pathway at a step downstream of Smo and upstream of the Gli transcription factors (reviewed in).
20544799	0.98	Dync2h1 yet acts genetically downstream of Kif3a and Ift88.
21305689	0.98	ift88, kif3a and dync2h1 mouse mutants.
30733609	0.98	Ift88, Ift72 and a gene that encodes a component of dynein-2 (Dync2h1) exhibited normal Axin2 mRNA expression and canonical WNT reporter activity .
31022843	0.98	ift88, kif3a, and dync2h1 were identified as critical components of Shh signaling through the primary cilium.
19718259	0.97	IFT88 and IFT172), or subunits of the motors that drive anterograde (Kif3a) or retrograde (Dync2h1) trafficking within cilia express canonical Wnt gene targets such as Axin2 or activate the BAT-gal reporter in the normal spatial pattern.
	0.97	IFT88, Kif3a or Dync2h1.
	0.96	Ift88 and Ift172 MEFs, Dync2h1 MEFs activated the SuperTOPFlash reporter normally in response to recombinant Wnt3a and this response was attenuated in the presence of the canonical Wnt inhibitor, Dkk1 (Figure 4C).
	0.95	Ift88, Ift172 and Dync2h1 MEFs respond normally to Wnt3a.
	0.94	Ift88, Ift172 and Dync2h1 mutant MEFs, exactly as seen in wild-type cells (Figure 4C).
	0.93	Ift88, Ift172 and Dync2h1 MEFs were completely non-responsive to Shh.
	0.85	Dync2h1 embryos generate cilia within 24 hours of culture, but not Ift172 or Ift88 mutant MEFs.
	0.74	Ift88, Ift172 and Dync2h1 MEFs fail to respond to Shh.
19223390	0.97	IFT88/polaris and Dnchc2 mutants, prompting us to look for similar changes in the abundance of the Gli3 isoforms in hitchhiker mutants.
	0.95	Dnchc2, IFT88/polaris, IFT172/wimple, Kif3a, Rpgrip1l/fantom and the chicken talpid3 mutant.
	0.94	IFT88/polaris/flexo, IFT172/wimple, Kif3a, Rpgrip1l/Fantom, Dync2h1/Dnchc2, IFT52/Ngd5, IFT57/hippi and Ofd1.
20395968	0.97	Ift88, as well as Dync2h1, the IFT-dedicated retrograde motor (Fig. 1).
	0.93	Ift88, Ift172 and Dync2h1 mutant mice and failed to find any alteration in either the domain or levels of Wnt activity.
21435552	0.97	Ift88, Ift172 and Dync2h1 show normal canonical Wnt responses in several assays, and that zebrafish lacking both maternal and zygotic Ift88 display defective Hh signaling, but no overt disruption in canonical Wnt signaling or PCP-guided convergent extension cell movements.
	0.96	Ift88, Ift52, Kif3a and Dync2h1 cause losses of ventral neuron cell types, consistent with deficient GliA, and polydactyly in the limb, consistent with reduced Gli3R.
21289087	0.97	Ift88 or Dync2h1 depletion, whereas Gli3 processing in the absence of Hh (into Gli3R) was only partially affected, suggesting that cilia facilitate but are not absolutely required for processing.
26542012	0.97	Ift88, Dync2h1, Ift172, Ift52, Ift57, Ift144, Ift25, and Ftm.
19517571	0.95	IFT88, IFT172), the anterograde motor protein Kif3A, and the retrograde IFT motor (Dnchc2) cause limb and neural tube patterning defects similar to phenotypes seen in Gli mutants (Huangfu et al., 2003; Huangfu and Anderson, 2005).
19000668	0.94	Ift88/polaris, Ift172/wimple, Ift52, as well as dynein heavy chain Dnchc2, or the Kif3A and Kif3B subunits of kinesin II, the proteolytic processing of Gli3 into Gli3R is compromised, and the reduced levels of Gli3R lead to extra digit formation (polydactyly).
19732765	0.84	Dync2h1 (dynein heavy chain) or flexo (IFT88/polaris), in which Shh signaling is decreased.
29548942	0.84	Ift88, Ift72, Dync2h1 and Kif3a, did not impact Wnt-responsiveness, as determined by LacZ expression in the BAT-gal reporter line.