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anti-Rat (Rattus) MAP3K7 Anticorps:
anti-Human MAP3K7 Anticorps:
anti-Mouse (Murine) MAP3K7 Anticorps:
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TAK1 regulates Nrf2 (Montrer GABPA Anticorps) through modulation of Keap-p62/SQSTM1 (Montrer SQSTM1 Anticorps) interaction. This regulation is important for homeostatic antioxidant protection in the intestinal epithelium.
Overexpression of TAK1 was strongly associated with positive lymph node metastasis in pancreatic ductal adenocarcinoma.
dysregulation of the TAK1 complex produces a close phenocopy of Frontometaphyseal Dysplasia caused by FLNA (Montrer FLNA Anticorps) mutations; furthermore, the pathogenesis of some of the filaminopathies caused by FLNA (Montrer FLNA Anticorps) mutations might be mediated by misregulation of signaling coordinated through the TAK1 signaling complex
although TAK1 is located at the crossroad of inflammation, immunity, and cancer, this study reports MAP3K7 mutations in a developmental disorder affecting mainly cartilage, bone, and heart
This study suggests that aberrant activity of TAK1 impairs autophagy and subsequently leads to alterations in the vitality of retinal pigment epithelial cells.
TAK1 may be an important factor involved in the pathogenesis of thyroid cancer, and targeted down-regulation of TAK1 may improve the prognosis of patients with thyroid cancer.
Loss of MAP3K7 are associated with esophageal squamous cell carcinoma.
This paper highlights that targeting the BMP and TGFbeta (Montrer TGFB1 Anticorps) type I and type II receptors causes a downregulation of XIAP (Montrer XIAP Anticorps), TAK1, and Id1 (Montrer ID1 Anticorps) leading to cell death of lung cancer cells.
Polyubiquitination of Transforming Growth Factor beta-activated Kinase 1 (TAK1) at Lysine 562 Residue Regulates TLR4 (Montrer TLR4 Anticorps)-mediated JNK (Montrer MAPK8 Anticorps) and p38 MAPK (Montrer MAPK14 Anticorps) Activation
The data emphasize the central role of TAK1 in controlling signaling cascades and functional responses in primary neutrophils, making it a promising target for therapeutic intervention in view of the role of neutrophils in chronic inflammatory conditions.
Tnfr1 (Montrer TNFRSF1A Anticorps) deletion partially restored thymic and lung macrophages.
TAK1 (Montrer NR2C2 Anticorps) is required for PPARgamma (Montrer PPARG Anticorps) transactivation and promotes PPARgamma (Montrer PPARG Anticorps) transcriptional activity synergistically with TAK1 binding protein 1 (TAB1 (Montrer TAB1 Anticorps)).
inhibition of TAK1 (Montrer NR2C2 Anticorps) triggered two caspase 8 (Montrer CASP8 Anticorps) activation pathways through the induction of RIP1 (Montrer RALBP1 Anticorps)-FADD (Montrer FADD Anticorps)-caspase 8 (Montrer CASP8 Anticorps) complex as well as FLIP cleavage/degradation.
Transforming growth factor-beta activated kinase 1 (TAK1) regulation of sterol-regulatory element-binding proteins (SREBPs) critically contributes to the maintenance of liver homeostasis to prevent steatosis, which is a potentially important mechanism to prevent hepatocellular carcinoma (HCC (Montrer FAM126A Anticorps)) development.
TAK1 (Montrer NR2C2 Anticorps) regulates Nrf2 (Montrer NFE2L2 Anticorps) through modulation of Keap-p62/SQSTM1 (Montrer SQSTM1 Anticorps) interaction. This regulation is important for homeostatic antioxidant protection in the intestinal epithelium.
Mekk1 (Montrer MAP2K1 Anticorps) (encoded by Map3k1 (Montrer MAP3K1 Anticorps)) signaling activates Mapks to regulate Cdkn1b (Montrer CDKN1B Anticorps) (encoding p27(Kip1 (Montrer CDKN1B Anticorps))) expression and p27(Kip1 (Montrer CDKN1B Anticorps))-dependent proliferative expansion in response to antigen.
TRADD (Montrer TRADD Anticorps) knockout blunts pressure overload-induced cardiac hypertrophy through mediating TAK1 (Montrer NR2C2 Anticorps)/p38 MAPK (Montrer MAPK14 Anticorps) but not AKT (Montrer AKT1 Anticorps) phosphorylation
this study demonstrates a pivotal role of TAK1 (Montrer NR2C2 Anticorps) in dendritic cells in controlling trichloroethylene-induced contact hypersensitivity response and suggests that targeting TAK1 (Montrer NR2C2 Anticorps) function in DCs may be a viable approach to preventing and treating TCE-related occupational health hazards
The E3 ligase TRIM8 (Montrer TRIM8 Anticorps) is a potent regulator that exacerbates steatohepatitis and metabolic disorders dependent on its binding and ubiquitinating capacity on transforming growth factor-beta-activated kinase 1.
Angiotensin-II up-regulates the Ampkalpha1 (Montrer PRKAA1 Anticorps) isoform in renal tissue. Ampkalpha1 (Montrer PRKAA1 Anticorps) participates in renal Tak1 (Montrer NR2C2 Anticorps) activation and Tak1 (Montrer NR2C2 Anticorps)-dependent signaling induced by angiotensin-II.
The protein encoded by this gene is a member of the serine/threonine protein kinase family. This kinase mediates the signaling transduction induced by TGF beta and morphogenetic protein (BMP), and controls a variety of cell functions including transcription regulation and apoptosis. In response to IL-1, this protein forms a kinase complex including TRAF6, MAP3K7P1/TAB1 and MAP3K7P2/TAB2\; this complex is required for the activation of nuclear factor kappa B. This kinase can also activate MAPK8/JNK, MAP2K4/MKK4, and thus plays a role in the cell response to environmental stresses. Four alternatively spliced transcript variants encoding distinct isoforms have been reported.
mitogen-activated protein kinase kinase kinase 7
, TGF-beta-activated kinase TAK1
, TGF-beta activated kinase 1
, TGF-beta-activated kinase 1
, transforming growth factor-beta-activated kinase 1
, mitogen activated protein kinase kinase kinase 7
, transforming growth factor beta-activated kinase 1