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Chicken Polyclonal Stratifin Primary Antibody für WB - ABIN2477187
dAlbis, Chanoine, Janmot, Mira, Couteaux: Muscle-specific response to thyroid hormone of myosin isoform transitions during rat postnatal development. in European journal of biochemistry / FEBS 1990
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Human Polyclonal Stratifin Primary Antibody für IHC (p), IHC - ABIN250903
Lodygin, Hermeking: The role of epigenetic inactivation of 14-3-3sigma in human cancer. in Cell research 2005
Human Monoclonal Stratifin Primary Antibody für IHC (p), IP - ABIN561091
Sousa, Zub, Aas, Hanssen-Bauer, Demirovic, Sarno, Tian, Liabakk, Slupphaug: An inverse switch in DNA base excision and strand break repair contributes to melphalan resistance in multiple myeloma cells. in PLoS ONE 2013
Cow (Bovine) Polyclonal Stratifin Primary Antibody für IHC, WB - ABIN2785886
Lu, Zhu, Wen, Yang, Shaw, Lammer, Finnell: Nicotinamide N-methyl transferase (NNMT) gene polymorphisms and risk for spina bifida. in Birth defects research. Part A, Clinical and molecular teratology 2008
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Review/Meta-analysis: 14-3-3 sigma promoter methylation may be associated with the carcinogenesis of breast cancer and might represent a useful blood-based biomarker for the clinical diagnosis of breast cancer.
This data indicates that 14-3-3sigma contributes to P-gp (zeige ABCB4 Antikörper) overexpression through interaction with PXR (zeige NR1I2 Antikörper) with rifampin and paclitaxel treatment.
The impact of AKT1 (zeige AKT1 Antikörper) on glucocorticoid receptor (GR (zeige NR3C1 Antikörper))-induced transcriptional activity in cooperation with phospho-serine/threonine-binding protein 14-3-3 (zeige YWHAQ Antikörper), was examined.
Data showed that 14-3-3s contributed to ionizing radiation (IR) resistance possibly by regulating cell cycle progression and non-homologous end joining repair of IR-induced DNA double strand breaks via regulating the expression of Chk2 (zeige CHEK2 Antikörper) and PARP1 (zeige PARP1 Antikörper). These findings suggest that 14-3-3s may be an upstream master regulator in chemo and radiation resistance and cancer cell survival.
Structural basis for the interaction of a human HSPB6 (zeige HSPB6 Antikörper) protein with the 14-3-3 (zeige YWHAQ Antikörper) universal signaling regulator has been reported.
Dual co-expression of human fetal Tau with PKA in Escherichia coli results in multisite Tau phosphorylation including also naturally occurring sites which were not previously considered in the context of 14-3-3 (zeige YWHAQ Antikörper) binding. Tau protein co-expressed with PKA displays tight functional interaction with 14-3-3 (zeige YWHAQ Antikörper) isoforms of a different type.
Data suggest that 14-3-3 sigma protein exhibits two individual secondary binding sites for peptide fragments of TAZ (zeige TAZ Antikörper) protein; these two pockets appear to be part of at least three physiologically relevant and structurally characterized 14-3-3 protein (zeige YWHAE Antikörper)-protein interaction interfaces.
These results suggest that SFN facilitates lung tumor development and progression. SFN appears to be a novel oncogene (zeige RAB1A Antikörper) with potential as a therapeutic target
SFN regulates cancer metabolic reprogramming. It opposes tumor-promoting metabolic programs by enhancing c-Myc (zeige MYC Antikörper) poly-ubiquitination and degradation. SFN suppresses cancer glycolysis, glutaminolysis, and mitochondrial biogenesis.
Data show that overexpression of the 14-3-3sigma isoform resulted in a disruption of the tubulin (zeige TUBB Antikörper) cytoskeleton mediated by binding Tau protein.
Loss of 14-3-3-sigma sensitizes mice to chemically-induced skin carcinogenesis. Therefore, 14-3-3-sigma may indeed represent a mediator of tumor suppression in the skin.
14-3-3sigma stabilizes a complex of soluble actin and intermediate filament to enable breast tumor invasion.
these data provides the first evidence that 14-3-3 sigma is a Smad3 (zeige SMAD3 Antikörper)-dependent target gene of TGF-beta1 (zeige TGFB1 Antikörper).
14-3-3sigma plays an important role in regulating mouse embryonic stem cell proliferation by binding and sequestering phosphorylated GSK-3beta and enhancing Wnt-signaled GSK-3beta inactivation.
study shows that p63 and 14-3-3sigma play opposing roles in the development of skin tumors and that the accumulation of p63 is essential for Ras/14-3-3sigma mutation-induced papilloma formation and squamous cell carcinoma carcinogenesis
Data show that endogenous 14-3-3sigma protein formed a complex with FOXO1 (zeige FOXO1 Antikörper) protein.
14-3-3 sigma is required for TGF-beta1 (zeige TGFB1 Antikörper)-mediated growth inhibition in mouse mammary epithelial cells.
14-3-3 sigma is needed for normal hair growth
14-3-3sigma is critical for regulating corneal epithelial proliferation and differentiation by regulating Notch (zeige NOTCH1 Antikörper) signaling activity.
14-3-3 (zeige YWHAQ Antikörper) can mediate the relocalization of nuclear ligands by several mechanisms that ensure complete sequestration of the bound 14-3-3 (zeige YWHAQ Antikörper) complex in the cytoplasm.
Adapter protein implicated in the regulation of a large spectrum of both general and specialized signaling pathways. Binds to a large number of partners, usually by recognition of a phosphoserine or phosphothreonine motif. Binding generally results in the modulation of the activity of the binding partner. When bound to KRT17, regulates protein synthesis and epithelial cell growth by stimulating Akt/mTOR pathway.
, 14-3-3 protein sigma
, epithelial cell marker protein 1
, 14-3-3 sigma protein
, tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, sigma polypeptide