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indicate an additional and specific role of this gene in the female reproductive tract, and furthermore reinforces ITIH5 as a putative candidate gene for MRKH syndrome.
ITIH5 may represent a novel modulator of TGF-beta superfamily signaling.
Results provide evidence that ITIH5 triggers a reprogramming of breast cancer cells through global epigenetic changes effecting DAPK1. ITIH5 may represent an ECM modulator in epithelial breast tissue mediating suppression of tumor initiating cancer cell characteristics which are thought being responsible for the metastasis of breast cancer.
Low ITIH5 expression is associated with liver metastasis in pancreatic cancer.
This is the first study so far showing a putative tumor suppressive function of ITIH5 in cervical carcinogenesis.
The current study describes a novel mechanism linking the TSG-6 transfer of the newly described HC5 to the HA-dependent control of cell phenotype. The interaction of HC5 with cell surface HA was essential for TGFbeta1-dependent differentiation of fibroblasts to myofibroblasts, highlighting its importance as a novel potential therapeutic target.
ITIH5 may be a novel putative tumor suppressor gene in NSCLC with a potential molecular significance in the squamoid ADC subtype and further clinical impact for risk stratification of adenocarcinoma patients.
Hence, we can strengthen the presumption that ITIH5 may constitute a novel regulatory molecule of the human skin that could play an important role in in fl ammation via its interaction with hyaluronic acid.
ITIH5 expression is decreased in gastric cancer and that low expression of this protein is associated with poor clinical outcome.
ITIH5 is a novel putative tumor suppressor gene in colon cancer with a potential impact in the CIMP-related pathway.
Tumor-specific methylation of the three-gene panel (ITIH5, DKK3, and RASSF1A) might be a valuable biomarker for the early detection of breast cancer.
provide evidence that down-regulation of ITIH5 by aberrant DNA hypermethylation may provoke invasive phenotypes in human bladder cancer
ITIH5 gene expression is regulated both by obesity and by the region between visceral and subcutaneous adipose tissue.
ITIH-5 is highly expressed in sc adipose tissue, increased in obesity, down regulated after weight loss, and associated with measures of body size and metabolism.
expression is consistantly lost or strongly downregulated in invasive ductal carcinoma; proposed that loss of ITIH5 expression may be involved in breast cancer development
Promoter methylation-mediated loss of ITIH5 expression is associated with unfavourable outcome in breast cancer patients.
Both ITIH5 protein expression and ITIH5 promoter methylation may serve as prognostic biomarkers, thereby helping improve clinical patient outcome.
This gene encodes a heavy chain component of one of the inter-alpha-trypsin inhibitor (ITI) family members. ITI proteins are involved in extracellular matrix stabilization and in the prevention of tumor metastasis. They are also structurally related plasma serine protease inhibitors and are composed of a light chain and varying numbers of heavy chains. This family member is thought to function as a tumor suppressor in breast and thyroid cancers. Alternative splicing results in multiple transcript variants.
ITI heavy chain H5
, inter-alpha trypsin inhibitor heavy chain precursor 5
, inter-alpha-inhibitor heavy chain 5
, inter-alpha-trypsin inhibitor heavy chain H5
, inter-alpha (globulin) inhibitor H5
, inter-alpha trypsin inhibitor heavy chain 5