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Human Polyclonal NR2C2 Primary Antibody für IF (p), IHC (p) - ABIN701185
Wang, Zhao, Yu, Feng, Zhang, Kou, Chu, Cui, Li, Zhang, Shen, Min: Regulation of steroid hormones and energy status with cysteamine and its effect on spermatogenesis. in Toxicology and applied pharmacology 2016
Show all 5 Pubmed References
Human Polyclonal NR2C2 Primary Antibody für WB - ABIN4357771
Liepelt, Mossanen, Denecke, Heymann, De Santis, Tacke, Marx, Ostareck, Ostareck-Lederer: Translation control of TAK1 mRNA by hnRNP K modulates LPS-induced macrophage activation. in RNA (New York, N.Y.) 2014
Show all 2 Pubmed References
Human Polyclonal NR2C2 Primary Antibody für ELISA, WB - ABIN251479
Omori, Matsumoto, Sanjo, Sato, Akira, Smart, Ninomiya-Tsuji: TAK1 is a master regulator of epidermal homeostasis involving skin inflammation and apoptosis. in The Journal of biological chemistry 2006
Human Polyclonal NR2C2 Primary Antibody für IF (p), IHC (p) - ABIN802023
Su, Zhou, Wang, Yang, Li, Yu, Li: The PPARβ/δ agonist GW501516 attenuates peritonitis in peritoneal fibrosis via inhibition of TAK1-NFκB pathway in rats. in Inflammation 2014
Human Polyclonal NR2C2 Primary Antibody für IF (p), IHC (p) - ABIN746333
Dvashi, Goldberg, Adir, Shapira, Pollack: TGF-?1 induced transdifferentiation of rpe cells is mediated by TAK1. in PLoS ONE 2015
TAK1, receptor-interacting kinase 1 (RIPK1) as well as canonical and non-canonical NF-kappaB signaling are differentially involved in SM-induced cell death in breast cancer cells.
Taken together, these results suggest that enterohemorrhagic Escherichia coli Tir negatively regulates proinflammatory responses by inhibiting the activation of TAK1, which is essential for immune evasion.
Authors reveal a propensity of the alternatively spliced TAK1 isoform TAK1E12 to cause drug resistance due to its activity in supporting EMT and NF-kappaB survival signaling.
Promotes clear cell renal carcinoma vasculogenic mimicry (VM) formation and its associated metastasis by modulating the miR490-3p-vimentin signals
The senescence-associated secretory phenotype is potentiated by feedforward regulatory mechanisms involving Zscan4 and TAK1.
Targeting the Cripto-1/TAK-1/NF-kappaB/Survivin pathway may be an effective approach to combat apoptosis resistance in cancer.
blockage of RhoA/ROCK repressed the TAK1/NOD2-mediated NF-kappaB pathway in HaCaT cells exposed to UVB.
Study found that TR4 might be able to function through activation of the AKT3 expression to drive the EMT phenotype and enhance the seminoma cell proliferation and invasion.
Altering TR4-ATF3 signaling increases the efficacy of cisplatin to suppress hepatocellular carcinoma growth/progression.
High TAK1 expression is associated with the progression of hepatocellular carcinoma.
Here, we report that Pseudomonas aeruginosa ExoY inhibits proinflammatory cytokine production through suppressing the activation of TAK1 as well as downstream NF-kappaB and mitogen-activated protein (MAP) kinases.
SIRT7 inhibits TR4 degradation by deacetylation of DDB1.
TR4 binds GR to play an important role in glucocorticoid-directed corticotroph tumor POMC regulation in addition to modulating glucocorticoid actions on other GR targets.
this study shows that TAP1 plays a novel role in the negative regulation of virus-triggered NF-kappaB signaling and the innate immune response by targeting the TAK1 complex
TAK1/TAB1 expression in non-small cell lung carcinoma tissue is significantly increased and closely associated with patient clinical prognosis.
miR-203 represses NF-kappaB signaling via targeting TAK1 and PI3KCA and miR-203 overexpression may contribute to the COPD initiation.
DK1 inhibits the formation of the TAK1-TAB2-TRAF6 complex and leads to the inhibition of TRAF6 ubiquitination.
IFIT5 promotes SeV-induced IKK phosphorylation and NF-kappaB activation by regulating the recruitment of IKK to TAK1.
USP18 negatively regulates NF-kappaB signaling by targeting TAK1 and NEMO for deubiquitination through distinct mechanisms.
Helicobacter pylori induces internalization of EGFR via novel TAK1-p38-serine activation pathway which is independent of HB-EGF.
Notch4 inhibited Mycobacterium tuberculosis-induced production of proinflammatory cytokines by interaction with TAK1 and inhibition of its activation.
our data suggest that NUMBL and TAK1 are reciprocally regulated and that NUMBL acts as an endogenous regulator of NF-kappaB signaling and osteoclastogenesis by targeting the TAK1-TRAF6-NEMO axis.
our findings demonstrate that CYLD mitigates Nonalcoholic steatohepatitis severity and identify the CYLD-TAK1 axis as a promising therapeutic target for management of the disease.
This study demonstrated that Myeloid-specific TAK1 deletion results in reduced brain monocyte infiltration and improved outcomes after stroke.
TNFalpha-induced phosphorylation of RIPK1 in the intermediate domain by TAK1 plays a key role in regulating the decision between three distinct mechanisms of cell death: necroptosis, RIPK1-independent and dependent apoptosis.
The results suggest that an intron-free Renilla luciferase reporter may provide a satisfactory internal control for TR4 at certain dose range. Findings advocate caution on the use of Renilla luciferase as an internal control in TR4-directed studies to avoid misleading data interpretation.
We conclude that TR4 is required for the normal differentiation and proliferation of erythroid cells, in addition to its previously characterized roles in embryonic and fetal globin gene repression
CNS-specific Tak1 deletion prevented ER-stress-induced hypothalamic leptin resistance and hyperphagic obesity under a high-fat diet (HFD). Thus, TAK1 is a crucial regulator of ER stress in vivo, which could be a target for alleviation of ER stress and its associated disease conditions.
this study shows that TAK1 negatively regulates lipopolysaccharide-induced cytokine secretion in myeloid cells by inhibiting MEKK3 activities
The present study demonstrates that TIPE2 acts as a novel negative regulator of inflammatory and immune responses through TAK1 signaling.
this study shows that increased activity of TAK1 contributes to diabetic nephropathy
Salidroside (SDS) downregulated protein expression of toll-like receptor 4 (TLR4) and CD14. SDS inhibited LPS-triggered phosphorylation of LPS-activated kinase 1 (TAK1), p38, c-Jun terminal kinase (JNK), and extracellular signal-regulated kinase (ERK).
miR-133a regulates TR4 expression in ox-LDL-induced mouse RAW 264.7 macrophages
TAK1 participates in intestinal integrity through separately modulating bacteria-derived reactive oxygen species and receptor-interacting protein kinase 3-dependent Paneth cell loss.
We confirmed that PGC-1b inhibited downstream inflammatory signals via binding with TAB1 and thus preventing TAB1/TAK1 binding and TAK1 activation.
Hepatocyte TRAF3 promotes liver steatosis and insulin resistance through targeting TAK1-dependent signaling.
Bacterial polysaccharide-responsive miR-150 and miR-143 RIPK2 and TAK1 to suppress NOD2-induced immunomodulators.
TR4-mediated enhancement of fatty acid synthesis in adipocytes requires increased expression of PC gene
Members of the nuclear hormone receptor family, such as NR2C2, act as ligand-activated transcription factors. The proteins have an N-terminal transactivation domain, a central DNA-binding domain with 2 zinc fingers, and a ligand-binding domain at the C terminus. The activated receptor/ligand complex is translocated to the nucleus where it binds to hormone response elements of target genes (Yoshikawa et al., 1996
Nuclear hormone receptor TR4
, TR4 nuclear hormone receptor
, nuclear receptor subfamily 2 group C member 2
, orphan nuclear receptor TAK1
, orphan nuclear receptor TR4
, testicular nuclear receptor 4
, testicular receptor 4
, TR4 orphan receptor
, TR4-NS orphan receptor
, orphan receptor TR4
, nuclear receptor subfamily 2, group H, member 2
, orphan receptor, TR4