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Human Polyclonal ACVR2B Primary Antibody für IHC (p), ELISA - ABIN542984
Iwata, Hacia, Suzuki, Sanchez-Lara, Urata, Chai: Modulation of noncanonical TGF-? signaling prevents cleft palate in Tgfbr2 mutant mice. in The Journal of clinical investigation 2012
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Human Polyclonal ACVR2B Primary Antibody für IHC (p), WB - ABIN391162
Harrison, Gray, Fischer, Donaldson, Choe, Vale: An activin mutant with disrupted ALK4 binding blocks signaling via type II receptors. in The Journal of biological chemistry 2004
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ActRIIB mRNA but not protein was decreased in skeletal muscle of obese compared with lean animals.
Study supported ACVR2B as the facilitator for clear cell kidney carcinoma (KIRC) development. Its up-regulation controls the growth, viability, and EMT-specific protein expressions of KIRC cells.
the A allele of genetic variant rs2276541 in ACVR2B is associated with lean muscle mass
TGF-beta receptor mediated telomerase inhibition, telomere shortening and breast cancer cell senescence.(
ActR-IIB is expressed in male germ cells and Sertoli cells.
Activin A inhibited signaling by BMP-6 and BMP-9 by competing for type 2 receptors ACVR2A and ACVR2B.
We found that the AAAAA, AGGAG, and AGGGA haplotypes in ACVR2B were associated with susceptibility to Premature Ovarian Failure when they also had at least one CATAG haplotype in ADAMTS19.
miR-21 interacts directly with the 3'-untranslated region of ACVR2B mRNA. Mechanical stretch suppressed ACVR2B protein levels in periodontal ligament stem cells. Gain- and loss of function of ACVR2B mediated the osteogenic differentiation of PDLSCs.
Adenomyotic tissues express high levels of myostatin, follistatin, and activin type II receptors.
Activin type IIB receptors are clearly demonstrable throughout the adult human hypothalamus and basal forebrain.
After eccentric exercise, postmenopausal women not using hormone therapy (HT) expressed lower levels of ActRIIb while postmenopausal women using HT showed a heightened response.
The interaction between all five miRNAs and ACVR2B was verified by an in vitro assay.
Mutations in Activin A Receptor Type IIB were identified in 4 of the 47 patients (8.5%) with heterotaxy syndrome. Our results expand the mutation spectrum of monogenic heterotaxy syndrome with associated cardiac anomalies.
discussion of crystal structure of kinase domain of ActRIIB; structural analysis may be of help in developing selective inhibitors [REVIEW]
Inhibition of negative regulators of skeletal muscle by a soluble form of activin type IIB receptor (ACE-031) increases muscle mass independent of fiber-type expression.
distribution in gestational tissues across human pregnancy and during labour
analysis of expression and cellular compartmentalization of the activin receptors ActRIIA, ActRIIB and ActRIB, the inhibin co-receptor (betaglycan), and activin signaling proteins Smads 2, 3 and 4, and growth regulatory role during lactation
Data indicate that activin A and activin receptors IIA and IIB may be involved in the regulation of germ cell proliferation in the human ovary during the period leading up to primordial follicle formation.
activin signaling via type II receptors requires a specific sequence for ALK4 binding
These results indicate that haplotype structure at the ACVR2B and follistatin loci may contribute to interindividual variation in skeletal muscle mass and strength, although these data indicate sex-specific relationships.
The high-resolution structure of human ActRIIB kinase domain in complex with adenine establishes the conserved bilobal architecture consistent with all other catalytic kinase domains.
Inhbaa signaled through Acvr2a over Acvr2b during zebrafish cardiac regeneration.
Roles in hindbrain and neural crest cell (NCC) patterning, in NCC derived pharyngeal arch cartilage and joint formation, and in tooth development.
The current study reveals that ActRIIB activation by activin A induces muscle catabolism primarily through the activation of p38beta MAPK-mediated catabolic signalling that activates the ubiquitin-proteasome pathway and the autophagy-lysosome pathway.
The endoplasmic reticulum stress stress and unfolded protein response are increased in mdx muscle. However, these processes are not distinctly improved by voluntary exercise or blocking activin receptor IIB ligands and thus do not appear to be optimal therapeutic choices for improving proteostasis in Duchenne muscular dystrophy.
Data, including data from studies using transgenic mice, suggest that osteoblasts deficient in Acvr2A exhibit un-characteristic features; osteoclasts deficient in Acvr2A or Acvr2B or both appear normal. Acvr2A-deficient mice exhibit significantly increased femoral trabecular bone volume at 6 weeks of age; Acvr2B-deficient mice exhibit no significant change in any bone parameter.
Differential muscle hypertrophy is associated with satellite cell numbers and Akt pathway activation following activin type IIB receptor inhibition in Mtm1
ActRIIB inhibition enhanced energy expenditure only at ambient temperature or in the cold, where nonshivering thermogenesis is minimal, suggesting that brown fat activation plays a prominent role in the metabolic actions of ActRIIB inhibition.
findings best fit a model in which BMP3, produced by mature bone cells, acts to reduce BMP signaling through Acvr2b in skeletal progenitor cells, limiting their differentiation to mature osteoblasts
Functional redundancy in osteoblast differentiation is observed between bone morphogenetic protein receptor BMPR-II and ActR-IIB.
Inhibition of activin receptor type IIB increases strength and lifespan in myotubularin-deficient mice.
Akt isoforms are not essential for for the ability of ActRIIB inhibition to regulate muscle size and function .
ActRIIB plays a role in the specification of left-sidedness in developing mice
Activin type IIB(ActRIIB) and its subfamily receptor, Activin type IIA (ActRIIA), cooperatively mediate the Gdf11 signal in patterning the axial vertebrae
ActRIIB is expressed in the early development of thymocytes.
genetic evidence strongly suggested that ActRIIB and Smad2 function in the same signaling pathway to regulate axial patterning and pancreas islet formation by means of a threshold mechanism.
expression of MSTN and its associated binding proteins can be modulated in adipose tissue and skeletal muscle by chronic obesity
Data suggest that BMP3 exerts its effects in the skeleton by altering signaling through ActRIIB in chondrocytes and the periosteum, and this results in defects in bone collar formation and late hypertrophic chondrocyte maturation.
Activins are dimeric growth and differentiation factors which belong to the transforming growth factor-beta (TGF-beta) superfamily of structurally related signaling proteins. Activins signal through a heteromeric complex of receptor serine kinases which include at least two type I (I and IB) and two type II (II and IIB) receptors. These receptors are all transmembrane proteins, composed of a ligand-binding extracellular domain with cysteine-rich region, a transmembrane domain, and a cytoplasmic domain with predicted serine/threonine specificity. Type I receptors are essential for signaling\; and type II receptors are required for binding ligands and for expression of type I receptors. Type I and II receptors form a stable complex after ligand binding, resulting in phosphorylation of type I receptors by type II receptors. Type II receptors are considered to be constitutively active kinases. This gene encodes activin A type IIB receptor, which displays a 3- to 4-fold higher affinity for the ligand than activin A type II receptor.
activin A receptor, type IIB
, activin receptor type IIB
, activin receptor type-2B-like
, activin type IIB receptor
, activin receptor type-2B
, testicular activin receptor IIB
, ActRIIB type II activin receptor B
, Activine receptor 2b (transmembrane serine kinase)
, activin receptor IIB