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Human Polyclonal TFF1 Primary Antibody for IHC, IHC (p) - ABIN4358634
Pontén, Jirström, Uhlen: The Human Protein Atlas--a tool for pathology. in The Journal of pathology 2008
Show all 4 Pubmed References
Human Monoclonal TFF1 Primary Antibody for ELISA, WB - ABIN563164
Kam, Hennessy, Chua, Gan, Philp, Hon, Lai, Chan, Ong, Wong, Lim, Ling, Tan, Tan, Ho, Kon: Characterization of the human gastric fluid proteome reveals distinct pH-dependent protein profiles: implications for biomarker studies. in Journal of proteome research 2011
Human Monoclonal TFF1 Primary Antibody for ELISA, WB - ABIN563163
Iorns, Martens-de Kemp, Lord, Ashworth: CRK7 modifies the MAPK pathway and influences the response to endocrine therapy. in Carcinogenesis 2009
Study findings demonstrate a functional role of TFF1 in suppressing gastric tumorigenesis by impeding the IL6-STAT3 pro-inflammatory signaling axis.
This study indicates that the acquisition of TFF1 expression is an early event in pancreatic carcinogenesis and that TFF1 might act as a tumor suppressor to prevent EMT and the invasive transformation of PanIN.
Study indicates that loss of TFF1 promotes the aberrant overexpression of HOXA10 and miR-196b by demethylation of the HOXA10 promoter, which provides a new perspective of TFF1/HOXA10/miR-196b functions in human gastric cancer.
TFF1 is responsible for liver regeneration after liver injury by promoting the differentiation of hepatic progenitor cells (HPC) into a biliary lineage and inhibiting HPC differentiation into a hepatic lineage.
our findings demonstrate overexpression of TIMP1 in mouse and human gastric cancers through NF-kB-dependent mechanism. We also show that TFF1 suppresses NF-kappaB and inhibits TIMP1-mediated proliferative potential in gastric cancer.
H. pylori upregulates GATA-5 mRNA levels after 6, 24, and 48 h of infection in gastric epithelial cells compared to uninfected cells, in parallel with a progressive increase in TFF1 mRNA levels.
Our study demonstrated that miR-632 promotes Gastric cancer progression by accelerating angiogenesis in a TFF1-dependent manner. Targeting of miR-632 may be a potential therapeutic approach for Gastric cancer patients.
Serum concentrations of TFF1 and TFF3 but not TFF2 are higher in women with breast cancer than in women without breast cancer.
results suggest that TFF1 and TFF3, but not TFF2, may have a role in breast tumor pathogenesis
Authors found that rs3761376 AA in the promoter region of TFF1, could reduce the expression of TFF1 by affecting the binding affinity of estrogen receptor 1 (ESR1, ERalpha), and thereby increased the risk of GC (1.29, 1.08-1.53).
Findings suggest that the hypoxic conditions, which can be induced by gastric injury, promote TFF1 up-regulation, strengthened by an auto-induction mechanism, and that the trefoil peptide takes part in the epithelial-mesenchymal transition events eventually triggered to repair the damage.
The urine TFF1 and TFF3 levels significantly increased with the progression of chronic kidney disease stages, but not the urine TFF2 levels.
Study shows that TFF1 expression is silenced in early phases of esophageal squamous cell carcinoma (ESCC) development, which seems to be mediated at least in part by promoter hypermethylation, and provides the basis for the use of TFF1 expression as a potential biomarker for early ESCC detection.
these data suggest that TFF1 might help cells to counteract Helicobacter colonization and the development of a chronic inflammation.
Co-expression of GKN2 and TFF1 massively suppressed the expression of positive cell cycle regulators and induced G1/S arrest, synergistically enhancing the inhibition of cell viability and proliferation of gastric cancer cells
The data suggest that the tumor suppressor activity of both RUNX1t1 and TFF1 are mechanistically connected to CEBPB and that cross-regulation between CEBPB-RUNX1t1-TFF1 plays an important role in gastric carcinogenesis.
Low TFF1 expression is associated with retinoblastoma.
The results suggest that the analysis of expression of MUC5AC and TFF1 may be useful for differentiating sessile serrated adenomas/polyps (SSA/Ps) from hyperplastic polyps (HPs).
TFF1 displays a distinct protein expression pattern in the developing of airway remodeling due to Sulfur mustard inhalation and plays an important role in maintaining the airway epithelium function
we found TFF1 plays an oncogenic role in mucinous ovarian cancer
the Tg(Tff1-CreERT2;Tff2-rtTA;Tff3-Luc) strain can confer intermittent transgene expression to gastric epithelial cells that have undergone previous gene modification, and may be suitable to genetically model therapeutic intervention during development, tumorigenesis, and other genetically tractable diseases
The up-regulated expression of Tff1 is probably the result of a complex inflammatory process as its expression is induced by tumor necrosis factor alpha as well as interleukins 1beta and 17.
Loss of TFF1 could be a critical step in promoting the H. pylori-mediated oncogenic activation of beta-catenin and gastric tumorigenesis.
Findings underscore an important protective role of TFF1 in abrogating H. pylori-mediated inflammation, a crucial hallmark of gastric tumorigenesis. Loss of TFF1 expression could be an important step in H. pylori-mediated gastric carcinogenesis.
TFF1 and TFF3 peptides might be involved in the complex processes of nervous system development and differentiation and brain plasticity.
Loss of TFF1 promotes beta-catenin activation and gastric tumorigenesis through regulation of PP2A, a major regulator AKT-GSK3Beta signaling.
Loss of Tff1 and high expression of cox2 are associated with gastric adenomas.
increased oncogenic potential of MCF7 cells in the absence of TFF1 was confirmed in vivo in nude mice
loss of TFF1 leads to activation of IKK complex-regulated NF-kappaB transcription factors and is an important event in shaping the NF-kappaB-mediated inflammatory response during the progression to gastric tumorigenesis
Initiation of antral gastric cancer is associated with progressive epigenetic silencing of TFF1, which can be suppressed by the hormone gastrin.
Studies indicate that TFF1-knockout mice demonstrate amplification and invasiveness of gastric stem/progenitor cells.
gene activation mediated by SHP2 and STAT pathways in gp130 mutant mice
Estrogen acts directly on the developing vagina in the permanent induction of TFF1 gene expression. TFF1 may be a useful marker for developmental estrogenization syndrome of the mouse vagina.
The results presented indicate for the first time that allergen exposure leads to the trans-differentiation of Clara cells toward a TFF1-expressing mucous phenotype.
This study shows that the progenitors of pit and gland mucous cells contribute to gastric carcinogenesis in the pyloric antrum of TFF1 knockout mice.
expression of xP1-L was detected in stage 41/42 tadpoles; in situ hybridization showed that xP1-L was localized to surface mucous cells of the larval stomach
Colon from infected swine had increased expression of MUC5AC and TFF1 relative to controls.
Weaning was not associated with fifferential TFF1 expression in the distal jejunum and ileum.
Members of the trefoil family are characterized by having at least one copy of the trefoil motif, a 40-amino acid domain that contains three conserved disulfides. They are stable secretory proteins expressed in gastrointestinal mucosa. Their functions are not defined, but they may protect the mucosa from insults, stabilize the mucus layer, and affect healing of the epithelium. This gene, which is expressed in the gastric mucosa, has also been studied because of its expression in human tumors. This gene and two other related trefoil family member genes are found in a cluster on chromosome 21.
breast cancer estrogen-inducible protein
, breast cancer estrogen-inducible sequence
, gastrointestinal trefoil protein pS2
, polypeptide P1.A
, protein pS2
, P-domain peptide pS2 gene product homolog
, putative gastrointestinal growth factor xP1
, trefoil factor 1 (breast cancer, estrogen-inducible sequence expressed in)
, trefoil factor family peptide 1
, trefoil factor 1
, P-domain peptide