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TL1A (zeige TNFSF15 Proteine) modulated Rheumatoid arthritis-fibroblast-like synoviocytes migration and Indian hedgehog signaling pathway using TNFR2 (zeige TNFRSF1B Proteine).
Association of pathogenic variants in IHH with short stature with nonspecific skeletal abnormalities and a frequent cause of growth disorder, with a preliminary good response to rhGH.
Studies suggest significance of other signaling aside from hedgehog (zeige SHH Proteine) in the pathogenesis of basal cell carcinoma (BCC) of the skin.
Gorlin syndrome-derived induced pluripotent stem cells (iPSCs) expressed lower basal levels than control iPSCs of the genes encoding the Hh ligands Indian Hedgehog (IHH) and Sonic Hedgehog (SHH (zeige SHH Proteine)).
Hedgehog (zeige SHH Proteine) pathway activation in T-cell acute lymphoblastic leukemia predicts response to SMO and GLI1 (zeige GLI1 Proteine) inhibitors.
CLIC4 (zeige CLIC4 Proteine) and Ihh could serve as biological markers for the progression, metastasis and/or invasiveness of pancreatic ductal adenocarcinoma.
The serum levels of IHH and SHH (zeige SHH Proteine) were significantly higher in autistic subjects than those of control subjects. The findings support a correlation between SHH (zeige SHH Proteine), IHH and BDNF (zeige BDNF Proteine) in autistic children, suggesting their pathological role in autism.
Our results show for the first time that Indian hedgehog does not cause extracellular matrix degradation in healthy ex vivo cartilage or in the presence of IL-1beta (zeige IL1B Proteine)
The Annexin a2 (zeige ANXA2 Proteine) Promotes Development in Arthritis through Neovascularization by Amplification Hedgehog (zeige SHH Proteine) Pathway.
Studies indicate that the hedgehog (zeige SHH Proteine) (Hh) signaling pathway has become one of the most studied potential therapeutic targets in hematological malignancies.
This work reveals the molecular function of Hedgehog (zeige SHH Proteine) signaling in extrinsic sheath tissues for tendon repair.
melatonin not only elevated progesterone (P) secretion, but also upregulated expressions of StAR and Cyp11a1 (zeige CYP11A1 Proteine) and also had an increased Ihh expression in endometrium.
loss of Spop, but not Spopl (zeige SPOPL Proteine), disrupts chondrocyte hypertrophy and osteoblast differentiation in the mouse, suggesting the requirement for Spop-mediated protein degradation in mouse skeletal development; overexpressed Spop targets both Gli3FL (zeige GLI3 Proteine) and Gli3R for ubiquitination and degradation and Spop is an important positive regulator of Ihh signaling and skeletal development
Ihh is regulated by at least 9 enhancers with individual tissue specificities in the digit anlagen, growth plates, skull sutures and fingertips. Consecutive deletions, resulting in growth defects of the skull and long bones, showed that these enhancers function in an additive manner. Duplications caused dose-dependent upregulation and misexpression of Ihh, abnormal phalanges, fusion of sutures and syndactyly.
GPC6 (zeige GPC6 Proteine) stimulates Hh signaling by binding to Hh and Ptc1 (zeige PTCH1 Proteine) at the cilium and increasing the interaction of the receptor and ligand to promote the growth of developing long bones.
An accelerated hypertrophic differentiation caused by a disturbed Ihh-PTHrP signaling pathway may lead to a higher bone mineral density in the vertebral bodies of newborn Col (zeige HDAC1 Proteine) IX -/- mice and, as a result, to the early onset of disc degeneration.
findings thus demonstrate that augmented Ihh signaling is detrimental to craniofacial development, and that finely tuned Ihh signaling is critical for temporomandibular joint formation.
Ihh has an important role in regulating limb mesenchymal cell differentiation
Ihh and PTH1R (zeige PTH1R Proteine) signaling in limb mesenchyme are both essential to regulate proper development of digit structures, although they appear to use different mechanisms.
By a combination of embryological andmolecular approaches the results demonstrated that Indian hedgehog protein signaling drives the migration of neural crest cells by autocrine or paracrine mechanisms.
Considered collectively, the present study suggests that X-bhh evolutionally acquired the function to induce osteogenesis; however, the expression profile of X-bhh in epiphysis is related to the late development of endochondral ossification in X. laevis.
Data indicate that SRY-box containing gene 4 protein (Sox4) is required to limit the extent of Hedgehog (zeige SHH Proteine) (Hh) signaling during eye development.
Cxcr4a is required for Hh-dependent cell proliferation but not for Hh-dependent patterning
Data showe that hedgehog (Hh) signaling regulates the expression of pth2 transcripts.
This gene encodes a member of the hedgehog family of secreted signaling molecules. Hedgehog proteins are essential regulators of a variety of developmental processes including growth, patterning and morphogenesis. The encoded protein specifically plays a role in bone growth an differentiation. Mutations in this gene are the cause of brachydactyly type A1 which is characterized by shortening or malformation of the phalanges. Mutations in this gene are also the cause of acrocapitofemoral dysplasia.
Indian hedgehog homolog
, Indian hedgehog
, indian hedgehog protein-like
, indian hedgehog protein
, banded hedgehog protein
, indian hedgehog homolog
, echidna hedgehog protein
, indian hedgehog B protein