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NOMPB is required for the assembly of sensory cilia but not for the extension or function of the sperm flagellum.
Tg737 regulates a Wnt (Montrer WNT2 Protéines)/beta-catenin (Montrer CTNNB1 Protéines)/Snail (Montrer SNAI1 Protéines)-HNF4alpha (Montrer HNF4A Protéines) negative feedback circuit, thereby blocking EMT (Montrer ITK Protéines) and the malignant transformation of liver stem cells to liver cancer stem cells.
genetically ablated Kif3a, Ift88, and Ttc21b in a series of specific spatiotemporal domains. The resulting phenotypes allow us to draw several conclusions. First, we conclude that the Ttc21b cortical phenotype is not due to the activity of Ttc21b within the brain itself
In order to evaluate the function of IFT88 in regulating craniofacial development, we generated Wnt1 (Montrer WNT1 Protéines)-Cre;Ift88fl/fl mice to eliminate Ift88 specifically in cranial neural crest (CNC) cells. Wnt1 (Montrer WNT1 Protéines)-Cre;Ift88fl/flpups died at birth due to severe craniofacial defects including bilateral cleft lip and palate and tongue agenesis, following the loss of the primary cilia in the CNC-derived palatal mesenchyme
IFT88 influences chondrocyte actin organization and biomechanics.
These data indicate that TGF-beta (Montrer TGFB1 Protéines) regulates Ift88 gene expression at least in part via posttrascriptional manner.
Results suggest that EGF (Montrer EGF Protéines) exerts mitogenic effects in the orpk cilia (-) cells via activation of growth-associated amiloride-sensitive NHEs and ERK (Montrer EPHB2 Protéines).
We propose that Ift88 and primary cilia regulate expression of Sfrp5 (Montrer SFRP5 Protéines) and Wnt (Montrer WNT2 Protéines) signaling pathways in growth plate via regulation of Ihh (Montrer IHH Protéines) signaling.
Knockout of Bbs7 (Montrer BBS7 Protéines) combined with a hypomorphic Ift88 allele (orpk as a model for Shh (Montrer SHH Protéines) dysfuction) results in embryonic lethality with e12.5 embryos having exencephaly, pericardial edema, cleft palate and abnormal limb development.
Data show that IFT88 is present in the Golgi of spermatids, that the microtubule-associated golgin GMAP210 and IFT88 participate in acrosome, HTCA, and tail biogenesis.
Epidermal cilia function was analyzed using conditional alleles of the ciliogenic genes Ift88 and Kif3a (Montrer KIF3A Protéines).
BFGF (Montrer FGF2 Protéines) also upregulated the mRNA and protein expression of IFT88 in primary cultured chondrocytes.
Data suggest that the function of the fusion transcript crystallin, lambda 1 protein - intraflagellar transport 88 (CRYL1 (Montrer CRYL1 Protéines)-IFT88) is closed to CRYL1 (Montrer CRYL1 Protéines) because it contained most of domain of CRYL1 (Montrer CRYL1 Protéines).
multivariate Cox (Montrer COX8A Protéines) regression analyses demonstrated that Tg737 expression was an independent factor for predicting the overall survival of hepatocellular carcinoma patients
MiR (Montrer MLXIP Protéines)-548a-5p negatively regulates the tumor inhibitor gene Tg737 and promotes tumorigenesis in vitro and in vivo, indicating its potential as a novel therapeutic target for hepatocellular carcinoma.
subtle regulation of IFT and associated cilia structure, tunes the wnt (Montrer WNT2 Protéines) response controlling stem cell differentiation.
this work suggests that Tg737 is involved in the invasion and migration of hepatoma cells under hypoxia, with the involvement of the polycystin-1 (Montrer PKD1 Protéines), IL-8 (Montrer IL8 Protéines), and TGF-beta1 (Montrer TGFB1 Protéines) signaling pathway
A mutation in IFT88 causes a hitherto unknown human ciliopathy.
Data show that IFT88 depletion induces mitotic defects in human cultured cells, in kidney cells from the IFT88 mouse mutant Tg737(orpk) and in zebrafish embryos.
The results indicate that loss of heterozygosity of the tumor suppressor gene Tg737 may play an important role in the carcinogenetic mechanism of liver cancer stem cells.
IFT88 is a centrosomal protein regulating G1-S transition in non-ciliated cells.
This gene encodes a member of the tetratrico peptide repeat (TPR) family. Mutations of a similar gene in mouse can cause polycystic kidney disease. Two transcript variants encoding distinct isoforms have been identified for this gene.
intraflagellar transport protein 88 homolog
, intraflagellar transport 88 homolog (Chlamydomonas)
, TPR repeat protein 10
, intraflagellar transport 88 homolog
, recessive polycystic kidney disease protein Tg737
, tetratricopeptide repeat domain 10
, tetratricopeptide repeat protein 10
, transgene insert site 737, insertional mutation, polycystic kidney disease
, polaris homolog
, probe hTg737 (polycystic kidney disease, autosomal recessive)
, recessive polycystic kidney disease protein Tg737 homolog