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Results show that Trps1 regulates multidrug sensitivity of lung cancer cells. Also, Trps1 induces MGMT transcription through binding to its promoter region. These data indicate that multidrug resistance of lung cancer cells is partly associated with Trps1-regulated MGMT gene transcription.
Study provide a novel mechanistic insight into the growth-regulatory role of TRPS1-USP4-HDAC2 axis by providing evidence that TRPS1 recruits USP4 to deubiquitinate and stabilize HDAC2. This is the first example of the non-transcription factor function of GATA transcription factor which affects the ubiquitination and transcription repressive function of HDAC2, acetylation of H4K16, and the deubiquitinase function of USP4.
study provides detailed mechanistic insights into CSC functions and tumor initiation by the TRPS1-SOX2 axis
Our data suggest that TRPS1 is an important ER-associated transcriptional repressor that regulates cell proliferation, chromatin acetylation and ER binding at the chromatin of cis-regulatory elements
TRPS1 is an epigenetic regulator of YAP activity in breast cancer
In Pseudohypoparathyroidism, mutations were found in PRKAR1A, PDE4D, TRPS1, and PTHLH.
Two Pakistani families with sequence variants in GDF5 and TRPS1 causing brachydactyly type C and tricho-rhino-phalangeal syndrome type III are described.
The results of this study indicated a prominent role of TRPS1 in subependymoma development.
Results showed that TRPS1 along with GATA3 are distinctively overexpressed in breast cancer (BC) among all GATA family members and predict better survival in patients with BC. TRPS1 is then a distinctive biomarker and essential prognostic factor in BC.
Downregulation of the TRPS1 protein, which is a transcriptional target of hsa-miR-26b-5p, was associated with radiation exposure.
The first patient has a novel heterozygous two-base-pair deletion of nucleotides at 3198-3199 (c.3198-3199delAT) in the TRPS1 gene causing a translational frameshift and subsequent alternate stop codon. The second patient has a 3.08 million base-pair interstitial deletion at 8q23.3 (113,735,487-116,818,578), which includes the TRPS1 gene and CSMD3
the twins described by Fitzsimmons had heterozygous mutations in the SACS gene, the gene responsible for autosomal recessive spastic ataxia of Charlevoix Saguenay as well as a heterozygous mutation in the TRPS1, the gene responsible in Trichorhinophalangeal syndrome type 1A TBL1XR1 mutation was identified in the patient described in 2009 as contributing to his cognitive impairment and autistic features..
Clinically, three patients had TRPS I, two with multiple supernumerary teeth. The clinical impression was confirmed by a novel TRPS1 mutation.
in this kindred support the previous genotype-phenotype results suggesting that patients with more pronounced facial characteristics and more severe shortening of hands and feet are more likely to have mutation in exon 6 of TRPS1
Down-regulation of TRPS1 by miR-373, acting as a transcriptional activator, promotes epithelial-mesenchymal transition (EMT) and metastasis by repressing FOXA1 transcription, expanding upon its previously reported role as a transcription repressor.
TRPS1 gene was responsible for most of the TRPS phenotype
Data show that co-silencing of tricho-rhino-phalangeal-syndrome (TRPS1) and cathepsin D (Cath-D) in breast cancer cells (BCC) affects the transcription of cell cycle and proliferation.
Trps1 plays a crucial role in osteosarcoma angiogenesis, metastasis and clinical surgical stage.
Single nucleotide polymorphisms in TRPS1 gene is associated with Coronary Artery Disease.
Missense mutations are located exclusively in exon 6 and 7 of TRPS1 in patients with tricho-rhino-phalangeal syndrome.
our findings partially explain why patients with TRPS show a broad range of congenital cardiac defects, although Trps1 expression is observed in a more restricted fashion.
Taken together, these results show that hair follicle development in Trps1 KO embryos is impaired directly or indirectly by decreased Noggin expression.
association between SNP within TRPS1 and BMD
Trps1 acts as a regulator of hdac1 and hdac4 histone deacetylases during mitosis.
The loss of Trps1 suppresses ureteric bud branching because of the activation of TGF-beta signaling.
We found that Trps1 directly represses expression of the hair follicle stem cell regulator Sox9 to control proliferation of the follicle epithelium.
Trps1 is identified as a potent inhibitor of Dspp expression and the subsequent mineralization of dentin.
analysis of control of mesenchymal lineage progression by microRNAs targeting skeletal gene regulators Trps1 and Runx2
These observations underscore the indispensable role played by Trps1 in normal temporomandibular joint development.
Genetic variation in TRPS1 may regulate hip geometry as well as bone mineral density
Trps1 activates a network of secreted Wnt inhibitors and transcription factors crucial to vibrissa follicle morphogenesis.
Trps1 binds to the P2 promoter of the Runx1 gene and down-regulates Runx1 expression, which is necessary for normal cartilage formation.
Only missense mutations in exon 6 of the TRPS1 gene are responsible for the severe form of TRPS
Trps1 haploinsufficiency enhances TGF-beta1-induced epithelial-to-mesenchymal transition (EMT) and tubulointerstitial fibrosis by modulating the amount of Smad7 through Arkadia/ubiquitin-mediated degradation.
Results implicate TRPS1 in regulation of bone and hair development and suggest that skeletal abnormalities emphasized in descriptions of TRPS are only the extreme manifestations of a generalized bone dysplasia.
expression of Trps1 during mouse embryonic development
TRPS1 activity is regulated by RNF4
Trps1 as a novel regulator of chondrocytes proliferation and survival through the control of Stat3 expression.
Dynamic expression of Trps1 during hair follicle morphogenesis and cycling is reported.
association of Gdf5-mediated signaling pathways with Trps1 and the phenotypic changes of ATDC5 cells due to over-expression or suppression of Trps1
This gene encodes a transcription factor that represses GATA-regulated genes and binds to a dynein light chain protein. Binding of the encoded protein to the dynein light chain protein affects binding to GATA consensus sequences and suppresses its transcriptional activity. Defects in this gene are a cause of tricho-rhino-phalangeal syndrome (TRPS) types I-III.
trichorhinophalangeal syndrome I homolog
, zinc finger transcription factor Trps1
, tricho-rhino-phalangeal syndrome type I protein
, zinc finger protein GC79
, atypical GATA protein TRPS1