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1 PTPN1 haploinsufficiency causes a type 1 IFN-driven auto
2 PTPN1 is located in 20q13, a genomic region linked to ty
3 ein tyrosine phosphatase nonreceptor type 1 (PTPN1) and PTPN2, whose expression is significantly high
4 show that these perturbations, as well as a PTPN1/PTPN2 inhibitor, sensitize ovarian cancer cells to
6 KRAS, GRB2, PCK2, BCL2L1, INSL3, DOK3, and PTPN1 were among the most significantly upregulated gene
8 The protein tyrosine phosphatases PTPN2 and PTPN1 are central regulators of inflammation, and their
9 We find that constitutive deletion of both PTPN1 and PTPN2 leads to bone marrow hypoplasia and leth
11 phosphatase nonreceptor type 1, also called PTPN1) was also identified as a potential proximity fact
12 We replicated the ADO-EGR2, IRF8, and CEBPB-PTPN1 loci by genotyping 969 Iranian cases and 826 contr
13 ee new risk loci, IL1A-IL1B, IRF8, and CEBPB-PTPN1, with genome-wide significance (P < 5 x 10(-8)) by
17 nes (DEGs), KLF9, AMPK, FOXO3, PTX3, GADD45, PTPN1, CASP7, MAPK4, HSPA12A, and JAK-STAT were probably
18 the first intron of the PTP1B encoding gene PTPN1, correlating with an AR-mediated increase in RNA p
19 erase reporter assay revealed that the genes PTPN1, HOXA1, and TP53I11 were miR-210 target genes regu
21 omic loss-of-function screens, we identified PTPN1 and PTPN2 phosphatases as consistent top hits driv
22 of individuals heterozygous for mutations in PTPN1, encoding the protein-tyrosine phosphatase 1B (PTP
24 ee single nucleotide polymorphisms (SNPs) in PTPN1 were genotyped and assessed for association with I
25 We found ten novel or very rare variants in PTPN1 (frequency on gnomAD version 4.1.0 of <1.25 x 10:s
29 xample, a genome-wide significant locus near PTPN1 (dog-directed aggression) overlapped with human me
30 with SNPs spanning the 3' end of intron 1 of PTPN1 through intron 8 (P values ranging from 0.043 to 0
32 ast, there is no evidence for association of PTPN1 polymorphisms with acute insulin response (a measu
34 m signaling analysis showed that deletion of PTPN1 or PTPN2 induces resistance to crizotinib by hyper
35 istance to ALK TKIs showed downregulation of PTPN1 and PTPN2 associated with upregulation of SHP2 exp
36 genetic perturbations-including knockout of PTPN1 and ACTR8-that trigger this malignant cell state.
37 sted PTPN1 variants led to reduced levels of PTPN1 mRNA and PTP1B protein, and in-vitro assays demons
38 hed the AR as a transcriptional regulator of PTPN1 transcription and implicated PTP1B in a tumor-prom
39 ilibrium encompassing the coding sequence of PTPN1 were significantly associated with CorCP (P values
41 effects of miR-210, coordinate silencing of PTPN1, HOXA1, and TP53I11 dramatically decreased tumor c
42 tically inhibited the growth of wild-type or PTPN1/PTPN2 knock-out ALCL, where it reverted TKI resist
43 the EGFR phosphatase PTPN2 (and potentially PTPN1)-via ligation to the PTPN2 active site cysteine si
44 phosphatases, five of which - DUSP6, PPTC7, PTPN1, PTPN13 and PPP3CA - promote differentiation by ne
46 The protein-tyrosine phosphatase 1B (PTP1B; PTPN1) is an important regulator of mammalian metabolism
49 ent blood and fibroblasts showed that tested PTPN1 variants led to reduced levels of PTPN1 mRNA and P
50 re coamplified in metastatic tumors and that PTPN1 amplification was associated with a subset of high
51 genes in distinct in vivo contexts and that PTPN1 and PTPN2 have some functional redundancy importan
59 yrosine phosphatase (PTP)-1B, encoded by the PTPN1 gene, catalyzes the dephosphorylation of proteins
60 ms (SNPs) spanning 161 kb and containing the PTPN1 gene were genotyped and tested for association.
61 0.1 in a single haplotype block covering the PTPN1 genomic sequence show significant association with
63 DNA arrays to genotype 6 SNP markers in the PTPN1 gene and 10 mutations in the cystic fibrosis trans
68 response of CML cells to imatinib treatment: PTPN1, NF1, SMARCB1, and SMARCE1, and 5 regulators of th