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these data demonstrate that EC-derived jagged-2 activates Notch2 signaling in HSPCs to promote hematopoietic recovery and has potential as a therapeutic target to accelerate balanced hematopoietic reconstitution after myelosuppression.
A deficiency of KLF2 increased the expression of Notch ligand Jagged2 via hypoxia-inducible factor 1alpha (HIF-1alpha), which led to Th2 amplification.
silencing prevents Notch2-driven osteoclast development and bone destruction in multiple myeloma
Although Jag1 shares a high degree of homology with Jag2 in the ectodomain region, BACE1 fails to cleave Jag2 effectively, indicating a selective cleavage of Jag1.
Reducing Jagged 1 and 2 levels prevents cerebral arteriovenous malformations in matrix Gla protein deficiency.
these findings suggest that Jagged2 signaling can affect graft acceptance by upregulation of IL-6 and consequent resistance to Treg-cell suppression.
results demonstrate that maternal P4 levels during midpregnancy can inhibit the expression of Jagged2 and Notch1, which are involved in primordial folliculogenesis, in the mouse fetal ovary
These data suggest that Notch ligands are differentially regulated in DCs: Delta-like 4 is regulated by T helper cells and by pathogen-derived Th1 stimuli, whereas Jagged 2 is regulated by Th2 cells and pathogen-derived Th2-promoting stimuli.
novel Jagged2/miR-200-dependent pathway that mediates lung adenocarcinoma epithelial-to-mesenchymal transition and metastasis
Loss of Jagged2 is associated with craniofacial, limb, and T cell development.
expression pattern in antigen presenting cells
Notch ligands, including Delta-like1 and 3 and Jagged1 and Jagged2, show distinct expression patterns in the developing and adult brain overlapping that of Notch1
identification as substrated for presenilin-dependent gamma-secretase cleavage
Jagged2 stimulates the development of natural killer cells from Lin(-) Sca-1(+) c-kit(+) hematopoietic stem cells
DLL1, functions synergistically with JAG2 in regulating hair cell differentiation in the cochlea.
both Notch1 and 2 are required in the ectoderm to receive the Jagged2 signal; Notch receives this signal at an early stage in the developmental process and memory of this event is retained by the mesenchyme
Notch signalling, involving Notch1 and Jagged2 is required to regulate the number of Fgf8-expressing cells that comprise the apical ectodermal ridge, and this is important for the freeing of the digits during normal limb formation.
Jag2-Notch1 signaling is spatiotemporally regulated in the oral epithelia during palate development to prevent premature palatal shelf adhesion to other oral tissues and to facilitate normal adhesion between the elevated palatal shelves.
p63, and particularly the DeltaNp63 isoform, is essential for thymic development via enhanced expression of FgfR2 and Jag2.
Results suggest that Jagged2 plays an essential role for mandibular condylar cartilage morphogenesis and development.
In CL+/-P Malay patients, the prevalence of mutations in the Jagged2 gene was 12.5%. Three variants (g.19779C>T, g.19547G>A, and g.19712C>T) were identified in the Jagged2 gene among nonsyndromic CL+/-P and noncleft patients. Only g.19712C>T showed a significant association with nonsyndromic CL+/-P patients (P = .039).
these results show that the Notch signaling pathway in T cells is crucial for the induction of TH2-mediated allergic airway inflammation in an house dust mite -driven asthma model but that expression of Jagged 1 or Jagged 2 on DCs is not required
The authors present novel structures of human ligands Jagged2 and Delta-like4 and human Notch2, together with functional assays, which suggest that ligand-mediated coupling of membrane recognition and Notch binding is likely to be critical in establishing the optimal context for Notch signalling.
Immunohistochemistry showed a reverse correlation between MUC2 and Notch3 or Jagged1 (P = 0.033 and P = 0.005, respectively) and between MUC5AC and Jagged1 or Hes1
Jagged-2 enhances immunomodulatory activity in adipose derived mesenchymal stem cells
Increased expression of JAG2, a target of miR-1280, is associated with high metastatic dissemination at diagnosis and a poor outcome in medulloblastoma.
Results show that tumor cell migration, invasion, and metastasis are dependent on JAGGED2 independently of NOTCH activation.
This study demonistrated that NOTCH ligands JAG1 and JAG2 as critical pro-survival factors in childhood medulloblastoma.
Jagged2 expression status was closely correlated with important histopathologic characteristics (grades and stages) and the recurrence and metastasis of bladder urothelial carcinomas.
Notch-1 and Jagged-2 are not expressed in spastic colon segments, which may be associated with the pathogenesis of Hirschsprung disease.
JAG2-mediated Notch activation confers phenotypic and functional aspects of Langerhans cell histiocytosis to dendritic cells.
JAG2 is often expressed by CD138(+) primary cells. Our results indicate that spontaneous clonogenic growth of myeloma cells requires the expression of JAG2.
This study is the first illustration of Notch-1 and Jagged-2 expression in human tissues from non-cancerous disease.
hypoxia-induced Jagged2 activation in both tumor invasive front and normal bone stroma has a critical role in tumor progression and metastasis
The stromal cell-mediated antiapoptotic effect on B- ALL cells is mediated by Notch-3 and -4 or Jagged-1/-2 and DLL-1 in a synergistic manner.
hypoxic induction of JAG2 in tumor cells mediates a hypoxia-regulated cross-talk between tumor and endothelial cells.
we have investigated their influence on early human hematopoiesis and show that Jagged2 affects hematopoietic lineage decisions very similarly as Delta-like-1 and -4, but very different from Jagged1
Expression of Notch3 and Jagged2 were highly correlated in tongue carcinoma tissues.
Notch ligands Jagged1b and Jagged2b induce duct cell lineage in the liver and pancreas of the zebrafish.
Results indicate that Jagged-Notch signaling is required for segregation between wt1-expressing cells and differentiated steroidogenic tissue.
Expression of both jagged2 and jagged1b mRNA in the central nervous system suggested that they might be involved in control of differentiating neural progenitors.
Mice homozygous for a deletion in the Notch-interaction domain of Jag2 presented a variety of severe dental abnormalities.
Jagged and Delta ligands are functionally redundant or required in specific combinations in many differentiation processes
Jag2-mediated Notch signaling maintains proliferating neural progenitors and regulates cell diversity in the ventral spinal cord.
The Notch signaling pathway is an intercellular signaling mechanism that is essential for proper embryonic development. Members of the Notch gene family encode transmembrane receptors that are critical for various cell fate decisions. The protein encoded by this gene is one of several ligands that activate Notch and related receptors. Two transcript variants encoding different isoforms have been found for this gene.
, protein jagged-2-like
, protein jagged-2
, notch ligand