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TGFBI encodes an RGD-containing protein that binds to type I, II and IV collagens. Zusätzlich bieten wir Ihnen Transforming Growth Factor, beta-Induced, 68kDa Kits (70) und Transforming Growth Factor, beta-Induced, 68kDa Proteine (20) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 120 products:
Human Polyclonal TGFBI Primary Antibody für IHC, IHC (p) - ABIN4284120
Kashyap, Harsha, Renuse, Pawar, Sahasrabuddhe, Kim, Marimuthu, Keerthikumar, Muthusamy, Kandasamy, Subbannayya, Prasad, Mahmood, Chaerkady, Meltzer, Kumar, Rustgi, Pandey: SILAC-based quantitative proteomic approach to identify potential biomarkers from the esophageal squamous cell carcinoma secretome. in Cancer biology & therapy 2011
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Arabidopsis thaliana Polyclonal TGFBI Primary Antibody für WB - ABIN2712086
Speth, Willing, Rausch, Schneeberger, Laubinger: RACK1 scaffold proteins influence miRNA abundance in Arabidopsis. in The Plant journal : for cell and molecular biology 2013
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Human Polyclonal TGFBI Primary Antibody für ELISA, IHC - ABIN4284118
Zenteno, Correa-Gomez, Santacruz-Valdez, Suarez-Sanchez, Villanueva-Mendoza: Clinical and genetic features of TGFBI-linked corneal dystrophies in Mexican population: description of novel mutations and novel genotype-phenotype correlations. in Experimental eye research 2009
Human Polyclonal TGFBI Primary Antibody für ELISA, WB - ABIN563175
Han, Sim, Vora, Huang: A unique TGFBI protein in granular corneal dystrophy types 1 and 2. in Current eye research 2012
Human Polyclonal TGFBI Primary Antibody für WB - ABIN520880
Han, Sim, Vora, Huang: Unique TGFBI protein in lattice corneal dystrophy. in Investigative ophthalmology & visual science 2011
A novel heterozygous TGFBI mutation was identified in the proband, c.1673T>G in exon 12 that leads to (Leu558Arg) change at the protein level.
TGFBI and periostin (zeige POSTN Antikörper) act similarly in the heart in affecting fibrosis and disease responsiveness.
The p.(Val113Ile) mutation results in an alteration of the atypical LCD phenotype associated with the p.(Leu558Pro) mutation. This represents only the second report of the alteration of the phenotype of a TGFBI dystrophy by a second, non-homozygous pathogenic mutation, and thus provides insight into the phenotype-genotype correlation of the TGFBI dystrophies.
Our findings demonstrate that granular corneal dystrophy type 1 may present with a vortex pattern of anterior stromal deposits. Although this pattern of dystrophic deposits is not recognized by clinicians as a typical phenotype of GCD1, it is consistent with the production of the majority of the TGFBI protein by the corneal epithelium.
The right cornea showed a higher number of lattice lines than the left cornea. Molecular analysis involving bidirectional complete sequencing demonstrated a novel T621P mutation in exon 14 of TGFBI.
ig-h3, Peroxiredoxin-2 (zeige PRDX2 Antikörper), and NRF2 (zeige GABPA Antikörper) have roles in cervical carcinogenesis
LASIK surgery of granular corneal dystrophy type 2 patients leads to accumulation and differential proteolytic processing TGFBI protein.
High TGFBI expression in Esophageal squamous cell carcinoma is associated with hematogenous recurrence.
We observed that knockdown of Cul4A was associated with increased sensitivity to gemcitabine through upregulation of TGFBI in lung cancer cells.
TGFBIp expression is positively regulated by TGF-beta1 (zeige TGFB1 Antikörper) in corneal fibroblasts, whereas TGF-beta1 (zeige TGFB1 Antikörper)-induced miR (zeige MLXIP Antikörper)-21 and miR (zeige MLXIP Antikörper)-181a negatively regulate TGFBIp expression.
Data suggest that big-h3 protein (BIGH3 (zeige TGFB1 Antikörper)) acts as a tumor suppressor in the retina.
TGF-beta (zeige TGFB1 Antikörper)-induced matricellular protein-null lungs displayed diminished elastic recoil and gas exchange efficiency
the data suggest a model by which cytokine-induced Myt3 suppression leads to Tgfbi de-repression and subsequently to impaired islet-cell migration, revealing a novel role for Myt3 in regulating islet-cell migration.
Studies reveal that growth hormone (GH (zeige GH1 Antikörper))increases TGFBI (zeige TGFB1 Antikörper) expression in a mouse and rat models of diabetic nephropathy (DN) which correlate with clinical results, and suggest that this mechanism can explain the podocytes depletion in DN.
Tgfbi deficiency is associated with the degradation of cartilage matrix
The results support a novel inflammatory pathway for diabetic retinopathy. This pathway is initiated by TGFbeta (zeige TGFB1 Antikörper) released from macrophages, which promotes synthesis and release of BIGH3 (zeige TGFB1 Antikörper) protein by REC (zeige ZDHHC2 Antikörper) and REC (zeige ZDHHC2 Antikörper) apoptosis.
TGFBI is a potential risk gene for human diabetes.
High blood TGFBIp levels were observed in cecal ligation and puncture (CLP)-induced septic mice. The absence of the TGFBIp gene in mice attenuated CLP-induced sepsis.
Collectively, our findings indicate that betaig-h3 (zeige TGFB1 Antikörper) promotes the fibrogenic influence of TGFbeta (zeige TGFB1 Antikörper) signaling, neutralizing the prochondrogenic influence of the hypoxic-inducible factor 1 activated by the microenvironment of limb mesenchymal aggregates.
the observed effect of TGFBI on bone mass and bone size was largely caused by the effect of TGFBI on periosteal bone formation
This study shows that upregulation of bigh3 and bambia mRNA correlated with the process of fin regeneration and regulation of TGF-b signaling, suggesting a new role for these proteins.
Results describe the distribution of TGFBI in the developing skeletal muscle of zebrafish embryos, and use antisense morpholino oligonucleotides to investigate the function of the endogenous protein.
downregulation of CSD2 (zeige TGFB1 Antikörper) by the heat-inducible miR398 is required for thermotolerance in Arabidopsis.
Data indicate that in the MKK5 (zeige MAP2K5 Antikörper)-RNAi (RNA interference) lines, the induction of CSD1 and CSD2 (zeige TGFB1 Antikörper) as well as the activation of MKK5 (zeige MAP2K5 Antikörper) activity were completely arrested.
Data indicate that transgenic plants expressing miR398-resistant forms of CSD1, CSD2 (zeige TGFB1 Antikörper) and CCS (zeige CCS Antikörper) under the control of their native promoters are more sensitive to heat stress.
miR398 links expression of the three major chloroplast copper proteins, plastocyanin, CCS1 and Csd2 (zeige TGFB1 Antikörper), to copper availability.
CSD2 (zeige TGFB1 Antikörper) expression is fine-tuned by miR398-directed mRNA cleavage.
Results show that CSD1, but not CSD2 (zeige TGFB1 Antikörper), mRNA levels were negatively correlated with miR398 levels during ozone, salinity and biotic stress.
This gene encodes an RGD-containing protein that binds to type I, II and IV collagens. The RGD motif is found in many extracellular matrix proteins modulating cell adhesion and serves as a ligand recognition sequence for several integrins. This protein plays a role in cell-collagen interactions and may be involved in endochondrial bone formation in cartilage. The protein is induced by transforming growth factor-beta and acts to inhibit cell adhesion. Mutations in this gene are associated with multiple types of corneal dystrophy.
, transforming growth factor-beta-induced protein ig-h3
, RGD-containing collagen-associated protein
, beta ig-h3
, transforming growth factor, beta induced, 68 kDa
, transforming growth factor, beta induced
, Transforming growth factor-beta-induced protein ig-h3
, transforming growth factor induced protein