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NOMPB is required for the assembly of sensory cilia but not for the extension or function of the sperm flagellum.
The authors show that IFT88 interacts with DGKdelta, and is associated with COPII-coated vesicles at the the endoplasmic reticulum exit sites.
Tg737 regulates a Wnt/beta-catenin/Snail-HNF4alpha negative feedback circuit, thereby blocking EMT 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-Cre;Ift88fl/fl mice to eliminate Ift88 specifically in cranial neural crest (CNC) cells. Wnt1-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 regulates Ift88 gene expression at least in part via posttrascriptional manner.
Results suggest that EGF exerts mitogenic effects in the orpk cilia (-) cells via activation of growth-associated amiloride-sensitive NHEs and ERK.
We propose that Ift88 and primary cilia regulate expression of Sfrp5 and Wnt signaling pathways in growth plate via regulation of Ihh signaling.
Knockout of Bbs7 combined with a hypomorphic Ift88 allele (orpk as a model for Shh 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.
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.
is required for assembly of renal cilium.
The polycystic kidney disease proteins, polycystin-1, polycystin-2, polaris, and cystin, are co-localized in renal cilia.
Data suggest a dosage effect of Tg737 on the limb phenotypes in observed skeletal pathologic conditions.
identification of two mouse mutants, wimple (wim) and flexo (fxo), that lack ventral neural cell types and show other phenotypes characteristic of defects in Sonic hedgehog signalling
ORPK has a developmental role in kidney cilia length and number
polaris has a role in proper development of articular cartilage and growth plate
Ther intraflagellar transport component polaris localized to nascent centrioles before incorporation into cilia, and depletion of polaris blocked axoneme formation.
Study shows that genetic inactivation of a ciliary gene, Ift88, leads to misorientation of stereociliary bundles and to shortening and widening of the cochlea and its sensory organ, indicating a requirement for Ift88 in planar cell polarity regulation.
These observations suggest that the rare and unique combination of IFT88 alleles observed in this study provide insight into the physiological role of IFT88 in humans and the likely mechanism underlying retinal pathology in the pedigree with inherited retinal degeneration
IFT88/primary cilia play a role in metabolic reprogramming in thyroid cancer cells.
BFGF 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-IFT88) is closed to CRYL1 because it contained most of domain of CRYL1.
multivariate Cox regression analyses demonstrated that Tg737 expression was an independent factor for predicting the overall survival of hepatocellular carcinoma patients
MiR-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 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, IL-8, and TGF-beta1 signaling pathway
A mutation in IFT88 causes a hitherto unknown human ciliopathy.
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