Ignet

Gene Information

Gene symbol: M6PR

Gene name: mannose-6-phosphate receptor (cation dependent)

HGNC ID: 6752

Related Genes

#	Gene Symbol	Number of hits
1	CD4	1 hits
2	CD8A	1 hits
3	CTSB	1 hits
4	CTSD	1 hits
5	IGF2	1 hits
6	INS	1 hits

Related Sentences

#	PMID	Sentence
1	9278305	There was colocalization of the FITC-labeled Ags with early (cathepsin D) and late endosomal markers (anti-mannose-6-phosphate receptor), lysosomal markers (CD-63), and acidic compartment markers (3-(2,4-dinitroanilino)-3'-amino-N-methyldipropylamine) in the uninfected cells, but the level of colocalized Ag was reduced in the 43HIV cells and HIV-1BaL-infected monocytes.
2	17507477	Insulin-like growth factor II receptor-mediated intracellular retention of cathepsin B is essential for transformation of endothelial cells by Kaposi's sarcoma-associated herpesvirus.
3	17507477	Increased targeting of CTSB to endosomes was caused by the induction by KSHV of the expression of insulin-like growth factor-II receptor (IGF-IIR), a mannose-6-phosphate receptor (M6PR) that binds to cathepsins.
4	17507477	Inhibition of IGF-IIR/M6PR expression by siRNA released CTSB for secretion.
5	17507477	In contrast to the increased cathepsin secretion observed in most other tumors, viral inhibition of CTSB secretion via induction of an M6PR is crucial for the transformation of endothelial cells.
6	17507477	Insulin-like growth factor II receptor-mediated intracellular retention of cathepsin B is essential for transformation of endothelial cells by Kaposi's sarcoma-associated herpesvirus.
7	17507477	Increased targeting of CTSB to endosomes was caused by the induction by KSHV of the expression of insulin-like growth factor-II receptor (IGF-IIR), a mannose-6-phosphate receptor (M6PR) that binds to cathepsins.
8	17507477	Inhibition of IGF-IIR/M6PR expression by siRNA released CTSB for secretion.
9	17507477	In contrast to the increased cathepsin secretion observed in most other tumors, viral inhibition of CTSB secretion via induction of an M6PR is crucial for the transformation of endothelial cells.
10	17507477	Insulin-like growth factor II receptor-mediated intracellular retention of cathepsin B is essential for transformation of endothelial cells by Kaposi's sarcoma-associated herpesvirus.
11	17507477	Increased targeting of CTSB to endosomes was caused by the induction by KSHV of the expression of insulin-like growth factor-II receptor (IGF-IIR), a mannose-6-phosphate receptor (M6PR) that binds to cathepsins.
12	17507477	Inhibition of IGF-IIR/M6PR expression by siRNA released CTSB for secretion.
13	17507477	In contrast to the increased cathepsin secretion observed in most other tumors, viral inhibition of CTSB secretion via induction of an M6PR is crucial for the transformation of endothelial cells.
14	25990242	We demonstrate that M6PR-expression on CD8(+) T cell surfaces is dynamically regulated during LmOVA bacterial infection.
15	25990242	Notably, time-lapse, confocal microscopy and flow cytometry confirms that M6PR(low) effectors, but not M6PR(high) effectors, escape Gzm-B lethal-hit derived from CD4(+)25(+) Treg cells.
16	25990242	Adoptive cotransfer of M6PR(low) effectors and M6PR(high) effectors sorted from LmOVA-infected, congenic mice at the peak of CD8(+) T cell response, reveals that M6PR(low) effectors with the CD8(+) T cell memory precursor phenotype preferentially survive the CD8(+) T cell contraction and differentiate into functional, long-lasting memory CD8(+) T cells.
17	25990242	Taken together, our data provide the first evidence, to our knowledge, that selective M6PR down-regulation has a critical role in CD8(+) T cell survival, and our findings have implications for efficient vaccine design and immunotherapy.
18	25990242	We demonstrate that M6PR-expression on CD8(+) T cell surfaces is dynamically regulated during LmOVA bacterial infection.
19	25990242	Notably, time-lapse, confocal microscopy and flow cytometry confirms that M6PR(low) effectors, but not M6PR(high) effectors, escape Gzm-B lethal-hit derived from CD4(+)25(+) Treg cells.
20	25990242	Adoptive cotransfer of M6PR(low) effectors and M6PR(high) effectors sorted from LmOVA-infected, congenic mice at the peak of CD8(+) T cell response, reveals that M6PR(low) effectors with the CD8(+) T cell memory precursor phenotype preferentially survive the CD8(+) T cell contraction and differentiate into functional, long-lasting memory CD8(+) T cells.
21	25990242	Taken together, our data provide the first evidence, to our knowledge, that selective M6PR down-regulation has a critical role in CD8(+) T cell survival, and our findings have implications for efficient vaccine design and immunotherapy.
22	25990242	We demonstrate that M6PR-expression on CD8(+) T cell surfaces is dynamically regulated during LmOVA bacterial infection.
23	25990242	Notably, time-lapse, confocal microscopy and flow cytometry confirms that M6PR(low) effectors, but not M6PR(high) effectors, escape Gzm-B lethal-hit derived from CD4(+)25(+) Treg cells.
24	25990242	Adoptive cotransfer of M6PR(low) effectors and M6PR(high) effectors sorted from LmOVA-infected, congenic mice at the peak of CD8(+) T cell response, reveals that M6PR(low) effectors with the CD8(+) T cell memory precursor phenotype preferentially survive the CD8(+) T cell contraction and differentiate into functional, long-lasting memory CD8(+) T cells.
25	25990242	Taken together, our data provide the first evidence, to our knowledge, that selective M6PR down-regulation has a critical role in CD8(+) T cell survival, and our findings have implications for efficient vaccine design and immunotherapy.
26	25990242	We demonstrate that M6PR-expression on CD8(+) T cell surfaces is dynamically regulated during LmOVA bacterial infection.
27	25990242	Notably, time-lapse, confocal microscopy and flow cytometry confirms that M6PR(low) effectors, but not M6PR(high) effectors, escape Gzm-B lethal-hit derived from CD4(+)25(+) Treg cells.
28	25990242	Adoptive cotransfer of M6PR(low) effectors and M6PR(high) effectors sorted from LmOVA-infected, congenic mice at the peak of CD8(+) T cell response, reveals that M6PR(low) effectors with the CD8(+) T cell memory precursor phenotype preferentially survive the CD8(+) T cell contraction and differentiate into functional, long-lasting memory CD8(+) T cells.
29	25990242	Taken together, our data provide the first evidence, to our knowledge, that selective M6PR down-regulation has a critical role in CD8(+) T cell survival, and our findings have implications for efficient vaccine design and immunotherapy.