Ignet

Gene Information

Gene symbol: NOTCH3

Gene name: notch 3

HGNC ID: 7883

Synonyms: CASIL

Related Genes

#	Gene Symbol	Number of hits
1	APLP2	1 hits
2	CD4	1 hits
3	IL2RA	1 hits
4	JAG1	1 hits
5	JAG2	1 hits
6	PTCRA	1 hits
7	TNFRSF4	1 hits

Related Sentences

#	PMID	Sentence
1	12849365	Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL)and some forms of cerebral amyloid angiopathy have a genetic basis.
2	14568923	Thymic-derived dysregulated tolerance has been suggested to occur in type 1 diabetes via impaired generation of CD4(+)CD25(+) T regulatory cells, leading to autoimmune beta cell destruction.
3	14568923	In this study, we demonstrate that Notch3 expression is a characteristic feature of CD4(+)CD25(+) cells.
4	14568923	The failure to develop the disease is associated with an increase of CD4(+)CD25(+) T regulatory cells, accumulating in lymphoid organs, in pancreas infiltrates and paralleled by increased expression of IL-4 and IL-10.
5	14568923	Accordingly, CD4(+) T cells from Notch3-transgenic mice inhibit the development of hyperglycemia and insulitis when injected into streptozotocin-treated wild-type mice and display in vitro suppressive activity.
6	14568923	Thymic-derived dysregulated tolerance has been suggested to occur in type 1 diabetes via impaired generation of CD4(+)CD25(+) T regulatory cells, leading to autoimmune beta cell destruction.
7	14568923	In this study, we demonstrate that Notch3 expression is a characteristic feature of CD4(+)CD25(+) cells.
8	14568923	The failure to develop the disease is associated with an increase of CD4(+)CD25(+) T regulatory cells, accumulating in lymphoid organs, in pancreas infiltrates and paralleled by increased expression of IL-4 and IL-10.
9	14568923	Accordingly, CD4(+) T cells from Notch3-transgenic mice inhibit the development of hyperglycemia and insulitis when injected into streptozotocin-treated wild-type mice and display in vitro suppressive activity.
10	17081781	Cellular interactions promoting the in vivo expansion of CD4(+)CD25(+)Foxp3(+) regulatory T (Treg) cells for maintenance of immune tolerance remain poorly defined.
11	17081781	Here we report that mobilized Lin(-)Sca-1(+)c-kit(+) (LSK) hematopoietic progenitor cells (HPCs), unlike medullary hematopoietic stem cells (HSCs), selectively drove the direct, immediate expansion of functional host-derived Treg cells, thereby preventing the progression to overt spontaneous autoimmune diabetes in nonobese diabetic mice.
12	17081781	Treg cell expansion required cell-to-cell contact and Notch3 signaling, which was mediated selectively through the Notch ligand Jagged2 expressed by the multipotent HPC subset, as assessed by small interfering RNA (siRNA) silencing.
13	19461123	Notch3 and pTalpha/pre-TCR sustain the in vivo function of naturally occurring regulatory T cells.
14	19461123	Moreover, by using double mutant mice, with T cell-targeted constitutive activation of Notch3 in a pTalpha(-/-) background, we demonstrate that pTalpha deletion significantly counteracts the Notch3-dependent expansion, the increased FoxP3 expression and the enhanced in vitro activity of naturally occurring T(reg)s.
15	19461123	Notably, the absence of pTalpha also impairs the Notch3-dependent protection against experimentally induced autoimmune diabetes.
16	19461123	Collectively, our data suggest that pTalpha expression is required for the in vivo function of naturally occurring T(reg)s and that the activation of Notch3 signaling may positively regulate the function of this population, through the pTalpha/pre-T cell receptor pathway.
17	19461123	Notch3 and pTalpha/pre-TCR sustain the in vivo function of naturally occurring regulatory T cells.
18	19461123	Moreover, by using double mutant mice, with T cell-targeted constitutive activation of Notch3 in a pTalpha(-/-) background, we demonstrate that pTalpha deletion significantly counteracts the Notch3-dependent expansion, the increased FoxP3 expression and the enhanced in vitro activity of naturally occurring T(reg)s.
19	19461123	Notably, the absence of pTalpha also impairs the Notch3-dependent protection against experimentally induced autoimmune diabetes.
20	19461123	Collectively, our data suggest that pTalpha expression is required for the in vivo function of naturally occurring T(reg)s and that the activation of Notch3 signaling may positively regulate the function of this population, through the pTalpha/pre-T cell receptor pathway.
21	19461123	Notch3 and pTalpha/pre-TCR sustain the in vivo function of naturally occurring regulatory T cells.
22	19461123	Moreover, by using double mutant mice, with T cell-targeted constitutive activation of Notch3 in a pTalpha(-/-) background, we demonstrate that pTalpha deletion significantly counteracts the Notch3-dependent expansion, the increased FoxP3 expression and the enhanced in vitro activity of naturally occurring T(reg)s.
23	19461123	Notably, the absence of pTalpha also impairs the Notch3-dependent protection against experimentally induced autoimmune diabetes.
24	19461123	Collectively, our data suggest that pTalpha expression is required for the in vivo function of naturally occurring T(reg)s and that the activation of Notch3 signaling may positively regulate the function of this population, through the pTalpha/pre-T cell receptor pathway.
25	19461123	Notch3 and pTalpha/pre-TCR sustain the in vivo function of naturally occurring regulatory T cells.
26	19461123	Moreover, by using double mutant mice, with T cell-targeted constitutive activation of Notch3 in a pTalpha(-/-) background, we demonstrate that pTalpha deletion significantly counteracts the Notch3-dependent expansion, the increased FoxP3 expression and the enhanced in vitro activity of naturally occurring T(reg)s.
27	19461123	Notably, the absence of pTalpha also impairs the Notch3-dependent protection against experimentally induced autoimmune diabetes.
28	19461123	Collectively, our data suggest that pTalpha expression is required for the in vivo function of naturally occurring T(reg)s and that the activation of Notch3 signaling may positively regulate the function of this population, through the pTalpha/pre-T cell receptor pathway.
29	23630352	OX40L/Jagged1 cosignaling by GM-CSF-induced bone marrow-derived dendritic cells is required for the expansion of functional regulatory T cells.
30	23630352	Concurrent signaling induced by OX40L and Jagged1 via OX40 and Notch3 receptors expressed on Tregs was essential for the Treg expansion with sustained FoxP3 expression.
31	23630352	Adoptive transfer of only OX40L(+)Jagged1(+) BMDCs led to Treg expansion, increased production of IL-4 and IL-10, and suppression of EAT in the recipient mice.