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AGS (show JAG1 ELISA Kits) is caused by mutations in one of two genes, namely, JAG1 (show JAG1 ELISA Kits) or NOTCH2. These genes are part of the Notch (show NOTCH1 ELISA Kits) signaling pathway, which is involved in cell fate determination. JAG1 (show JAG1 ELISA Kits) mutations have been identified in 70-94% of individuals with clinically diagnosed AGS (show JAG1 ELISA Kits)
This is supported by the depletion of CTCF (show CTCF ELISA Kits) in glioblastoma cells affecting the expression levels of NOTCH2 as a target of miR (show MLXIP ELISA Kits)-181c. CONCLUSION: Together, our results point to the epigenetic role of CTCF (show CTCF ELISA Kits) in the regulation of microRNAs implicated in tumorigenesis
suggest that Notch2 has an essential role in the cell growth, invasion, and migration of SACC. Notch2 may therefore be a potential target gene for the treatment of SACC by interfering with cell growth and metastasis
Notch2 and Notch3 (show NOTCH3 ELISA Kits) inhibited both cell proliferation and cell apoptosis in BeWo and JAR (show MYO6 ELISA Kits) trophoblast cell lines.
A functional polymorphism in the premiR146a gene influences the prognosis of glioblastoma multiforme by interfering with the balance between Notch1 (show NOTCH1 ELISA Kits) and Notch2
Results suggest that Notch2 pathway and miR (show MLXIP ELISA Kits)-23b interplay in a reciprocal regulation loop in gastric cancer cells and this axis plays an important role in gastric carcinogenesis.
These findings suggested that the NOTCH2 signaling may confer aggressive behavior and immature morphology in human hepatocellular carcinoma cells.
Notch (show NOTCH1 ELISA Kits) signaling sustains chronic lymphocytic leukemia cell survival by promoting Mcl-1 (show MCL1 ELISA Kits) expression and eIF4E (show EIF4E ELISA Kits) activity, and given the oncogenic role of these factors, underscores the therapeutic potential of Notch (show NOTCH1 ELISA Kits) inhibition in chronic lymphocytic leukemia.
High Notch2 expression is associated with chronic myeloid leukemia (show BCL11A ELISA Kits).
miR (show MLXIP ELISA Kits)-191 represses proliferation in primary human fibroblasts via targeting multiple proto-oncogenes, including CDK9 (show CDK9 ELISA Kits), NOTCH2, and RPS6KA3 (show RPS6KA3 ELISA Kits).
In this study, authors use a smooth muscle-specific (show EIF3K ELISA Kits) deletion of Notch2 together with a global Notch3 (show NOTCH3 ELISA Kits) deletion to produce mice with combinations of mutant and wild-type Notch2/3 alleles in vascular smooth muscle cells
6955C-->T mutation in the Notch2 locus leading to cancellous and cortical bone osteopenia.
Data (including data from studies in transgenic/knockout mice) suggest deletion of Notch1 (show NOTCH1 ELISA Kits) in podocytes prevents diabetic nephropathy development and up-regulates Notch2 expression; overexpression of Notch2 does not promote diabetic nephropathy.
Expression of Notch1 and Notch2 was decreased in regenerated epidermis of wounds, where features of keratinocytes were altered. Notch1 and Notch2 down-regulation contributed to the induction of interleukin-36alpha expression.
data indicate distinct effects of Notch (show NOTCH1 ELISA Kits) signaling on invariant natural killer T cells in the thymus and liver, which are at least partly independent of RBP-j (show RBPJ ELISA Kits) in the thymus.
Notch1 (show NOTCH1 ELISA Kits) and Notch2 intracellular domains are functionally equivalent during development and carcinogenesis
NOTCH2 inhibits PDGF-B (show PDGFB ELISA Kits)-dependent proliferation and its expression is decreased by PDGF-B (show PDGFB ELISA Kits).
BTK (show BTK ELISA Kits) synergizes with Notch2 to govern marginal zone B cells in non-obese diabetic mice.
Surface expression of NOTCH2 was seen in specified E11 (show PDPN ELISA Kits) AGM (show IGFBP7 ELISA Kits) (CD45 (show PTPRC ELISA Kits)+VE-cadherin (show CDH5 ELISA Kits)+) hematopoietic progenitors. NOTCH (show NOTCH1 ELISA Kits) activation by Delta1 can increase long-term engrafting HSC (show FUT1 ELISA Kits) numbers from these cells.
Notch1 (show NOTCH1 ELISA Kits) is the primary receptor regulating intestinal stem cell function and Notch1 (show NOTCH1 ELISA Kits) and Notch2 together regulate epithelial cell proliferation, cell fate determination, and post-injury regeneration
bovine herpesvirus 1 ORF2 protein reduced the trans-activation potential of Notch1 (show NOTCH1 ELISA Kits) and Notch3 (show NOTCH3 ELISA Kits), suggesting that ORF2 interfered with the trans-activation potential of Notch (show NOTCH1 ELISA Kits).
DeltaC/Notch1a and Notch2 signaling is responsible for a survival signal provided by xanthophores to melanophores.
This gene encodes a member of the Notch family. Members of this Type 1 transmembrane protein family share structural characteristics including an extracellular domain consisting of multiple epidermal growth factor-like (EGF) repeats, and an intracellular domain consisting of multiple, different domain types. Notch family members play a role in a variety of developmental processes by controlling cell fate decisions. The Notch signaling network is an evolutionarily conserved intercellular signaling pathway which regulates interactions between physically adjacent cells. In Drosophilia, notch interaction with its cell-bound ligands (delta, serrate) establishes an intercellular signaling pathway that plays a key role in development. Homologues of the notch-ligands have also been identified in human, but precise interactions between these ligands and the human notch homologues remain to be determined. This protein is cleaved in the trans-Golgi network, and presented on the cell surface as a heterodimer. This protein functions as a receptor for membrane bound ligands, and may play a role in vascular, renal and hepatic development. Two transcript variants encoding different isoforms have been found for this gene.
, neurogenic locus notch homolog protein 2-like
, Notch homolog 2
, neurogenic locus notch homolog protein 2
, Motch B
, Notch gene homolog 2
, notch gene homolog 2
, notch receptor protein 6