Ignet

Gene Information

Gene symbol: SPG7

Gene name: spastic paraplegia 7 (pure and complicated autosomal recessive)

HGNC ID: 11237

Synonyms: CAR, SPG5C

Related Genes

#	Gene Symbol	Number of hits
1	CD80	1 hits
2	CD86	1 hits
3	CDH1	1 hits
4	FOS	1 hits
5	IFIH1	1 hits
6	JUN	1 hits
7	LTA	1 hits
8	MAPK1	1 hits
9	MAPK3	1 hits
10	MAPK8	1 hits
11	MUC1	1 hits
12	NAIP	1 hits
13	NOD1	1 hits
14	NOD2	1 hits
15	NOS2A	1 hits
16	PGLYRP1	1 hits
17	PTPN11	1 hits
18	S100A8	1 hits
19	TLR2	1 hits
20	TLR4	1 hits
21	TNF	1 hits
22	VWS	1 hits

Related Sentences

#	PMID	Sentence
1	19278729	Peptidoglycan (PGN), lipoteichoic acid (LTA), lipoprotein (LP), and DNA were also isolated from the bacteria, and used to stimulate BM-DCs.
2	19278729	Stimulation with TNF, S. gordonii, PGN, LTA, or LP all resulted in increased surface expression of MHCII, CD80, and CD86, compared to unstimulated BM-DCs.
3	19278729	Stimulation with S. gordonii elicited IL-6, IL-10, and IL-12p70 production from the BM-DCs, while stimulation with the bacterial components induced some or all of the three cytokines.
4	19278729	When BM-DCs were simultaneously stimulated with S. gordonii and TNF, a marginal increase in surface marker upregulation was observed, and the two stimuli synergized to elicit substantially greater quantities of IL-6, IL-10, and IL-12p70.
5	19278729	The effect of TNF was abolished when BM-DCs were obtained from mice deficient for either TNFR1 or TNFR2, and cytokine induction by S. gordonii was entirely dependent on functional MyD88.
6	19278729	Synergistic IL-10 induction by S. gordonii and TNF was not observed in TLR-2(-/-) BM-DCs, and TNF was found to cause TLR-2 upregulation, providing at least a partial mechanism for the observed synergy.
7	21188584	Bacterial cell wall polysaccharides, such as PGN, bind and activate TLR-2, NOD2 and PGRP on monocytes/macrophages and activate inflammation.
8	21188584	MTP, MDP, and lysine-less PGN bind to TLR-2, 87-113.
9	21450974	The objectives of this study were to examine the roles of mitogen-activated protein kinases (MAPKs) and transcription factors (nuclear factor-κB [NF-κB] and activating protein 1 [AP-1]) in peptidoglycan (PGN)-induced iNOS expression and NO production in macrophages.
10	21450974	PGN stimulates the activation of all three classes of MAPKs, extracellular signal-related kinase (ERK), c-Jun N-terminal kinase (JNK), and p38(mapk) in macrophages, albeit with differential activation kinetics.
11	21450974	Using a selective inhibitor of JNK (SP600125) and JNK1/2 small interfering RNA (siRNA) knocked-down macrophages, it was observed that PGN-induced iNOS and NO expression is significantly inhibited.
12	21450974	This suggested that JNK MAPK plays an essential role in PGN-induced iNOS expression and NO production.
13	21450974	In contrast, inhibition of the ERK pathway using PD98059 dose dependently enhanced PGN-induced iNOS expression and NO production.
14	21450974	PGN-induced ERK activation was attenuated in ERK1/2 siRNA knocked-down macrophages; however, NO and iNOS expression were significantly enhanced.
15	21450974	An electrophoretic mobility shift assay showed that SP600125 inhibited PGN-induced NF-κB and AP-1 activation, whereas inhibition of the ERK pathway enhanced NF-κB activation, but with no effect on AP-1.
16	21450974	These results indicate that the JNK MAPK positively regulate PGN-induced iNOS and NO expression by activating NF-κB and AP-1 transcription factors, whereas the ERK pathway plays a negative regulatory role via affecting NF-κB activity.
17	21450974	The objectives of this study were to examine the roles of mitogen-activated protein kinases (MAPKs) and transcription factors (nuclear factor-κB [NF-κB] and activating protein 1 [AP-1]) in peptidoglycan (PGN)-induced iNOS expression and NO production in macrophages.
18	21450974	PGN stimulates the activation of all three classes of MAPKs, extracellular signal-related kinase (ERK), c-Jun N-terminal kinase (JNK), and p38(mapk) in macrophages, albeit with differential activation kinetics.
19	21450974	Using a selective inhibitor of JNK (SP600125) and JNK1/2 small interfering RNA (siRNA) knocked-down macrophages, it was observed that PGN-induced iNOS and NO expression is significantly inhibited.
20	21450974	This suggested that JNK MAPK plays an essential role in PGN-induced iNOS expression and NO production.
21	21450974	In contrast, inhibition of the ERK pathway using PD98059 dose dependently enhanced PGN-induced iNOS expression and NO production.
22	21450974	PGN-induced ERK activation was attenuated in ERK1/2 siRNA knocked-down macrophages; however, NO and iNOS expression were significantly enhanced.
23	21450974	An electrophoretic mobility shift assay showed that SP600125 inhibited PGN-induced NF-κB and AP-1 activation, whereas inhibition of the ERK pathway enhanced NF-κB activation, but with no effect on AP-1.
24	21450974	These results indicate that the JNK MAPK positively regulate PGN-induced iNOS and NO expression by activating NF-κB and AP-1 transcription factors, whereas the ERK pathway plays a negative regulatory role via affecting NF-κB activity.
25	21450974	The objectives of this study were to examine the roles of mitogen-activated protein kinases (MAPKs) and transcription factors (nuclear factor-κB [NF-κB] and activating protein 1 [AP-1]) in peptidoglycan (PGN)-induced iNOS expression and NO production in macrophages.
26	21450974	PGN stimulates the activation of all three classes of MAPKs, extracellular signal-related kinase (ERK), c-Jun N-terminal kinase (JNK), and p38(mapk) in macrophages, albeit with differential activation kinetics.
27	21450974	Using a selective inhibitor of JNK (SP600125) and JNK1/2 small interfering RNA (siRNA) knocked-down macrophages, it was observed that PGN-induced iNOS and NO expression is significantly inhibited.
28	21450974	This suggested that JNK MAPK plays an essential role in PGN-induced iNOS expression and NO production.
29	21450974	In contrast, inhibition of the ERK pathway using PD98059 dose dependently enhanced PGN-induced iNOS expression and NO production.
30	21450974	PGN-induced ERK activation was attenuated in ERK1/2 siRNA knocked-down macrophages; however, NO and iNOS expression were significantly enhanced.
31	21450974	An electrophoretic mobility shift assay showed that SP600125 inhibited PGN-induced NF-κB and AP-1 activation, whereas inhibition of the ERK pathway enhanced NF-κB activation, but with no effect on AP-1.
32	21450974	These results indicate that the JNK MAPK positively regulate PGN-induced iNOS and NO expression by activating NF-κB and AP-1 transcription factors, whereas the ERK pathway plays a negative regulatory role via affecting NF-κB activity.
33	21450974	The objectives of this study were to examine the roles of mitogen-activated protein kinases (MAPKs) and transcription factors (nuclear factor-κB [NF-κB] and activating protein 1 [AP-1]) in peptidoglycan (PGN)-induced iNOS expression and NO production in macrophages.
34	21450974	PGN stimulates the activation of all three classes of MAPKs, extracellular signal-related kinase (ERK), c-Jun N-terminal kinase (JNK), and p38(mapk) in macrophages, albeit with differential activation kinetics.
35	21450974	Using a selective inhibitor of JNK (SP600125) and JNK1/2 small interfering RNA (siRNA) knocked-down macrophages, it was observed that PGN-induced iNOS and NO expression is significantly inhibited.
36	21450974	This suggested that JNK MAPK plays an essential role in PGN-induced iNOS expression and NO production.
37	21450974	In contrast, inhibition of the ERK pathway using PD98059 dose dependently enhanced PGN-induced iNOS expression and NO production.
38	21450974	PGN-induced ERK activation was attenuated in ERK1/2 siRNA knocked-down macrophages; however, NO and iNOS expression were significantly enhanced.
39	21450974	An electrophoretic mobility shift assay showed that SP600125 inhibited PGN-induced NF-κB and AP-1 activation, whereas inhibition of the ERK pathway enhanced NF-κB activation, but with no effect on AP-1.
40	21450974	These results indicate that the JNK MAPK positively regulate PGN-induced iNOS and NO expression by activating NF-κB and AP-1 transcription factors, whereas the ERK pathway plays a negative regulatory role via affecting NF-κB activity.
41	21450974	The objectives of this study were to examine the roles of mitogen-activated protein kinases (MAPKs) and transcription factors (nuclear factor-κB [NF-κB] and activating protein 1 [AP-1]) in peptidoglycan (PGN)-induced iNOS expression and NO production in macrophages.
42	21450974	PGN stimulates the activation of all three classes of MAPKs, extracellular signal-related kinase (ERK), c-Jun N-terminal kinase (JNK), and p38(mapk) in macrophages, albeit with differential activation kinetics.
43	21450974	Using a selective inhibitor of JNK (SP600125) and JNK1/2 small interfering RNA (siRNA) knocked-down macrophages, it was observed that PGN-induced iNOS and NO expression is significantly inhibited.
44	21450974	This suggested that JNK MAPK plays an essential role in PGN-induced iNOS expression and NO production.
45	21450974	In contrast, inhibition of the ERK pathway using PD98059 dose dependently enhanced PGN-induced iNOS expression and NO production.
46	21450974	PGN-induced ERK activation was attenuated in ERK1/2 siRNA knocked-down macrophages; however, NO and iNOS expression were significantly enhanced.
47	21450974	An electrophoretic mobility shift assay showed that SP600125 inhibited PGN-induced NF-κB and AP-1 activation, whereas inhibition of the ERK pathway enhanced NF-κB activation, but with no effect on AP-1.
48	21450974	These results indicate that the JNK MAPK positively regulate PGN-induced iNOS and NO expression by activating NF-κB and AP-1 transcription factors, whereas the ERK pathway plays a negative regulatory role via affecting NF-κB activity.
49	21450974	The objectives of this study were to examine the roles of mitogen-activated protein kinases (MAPKs) and transcription factors (nuclear factor-κB [NF-κB] and activating protein 1 [AP-1]) in peptidoglycan (PGN)-induced iNOS expression and NO production in macrophages.
50	21450974	PGN stimulates the activation of all three classes of MAPKs, extracellular signal-related kinase (ERK), c-Jun N-terminal kinase (JNK), and p38(mapk) in macrophages, albeit with differential activation kinetics.
51	21450974	Using a selective inhibitor of JNK (SP600125) and JNK1/2 small interfering RNA (siRNA) knocked-down macrophages, it was observed that PGN-induced iNOS and NO expression is significantly inhibited.
52	21450974	This suggested that JNK MAPK plays an essential role in PGN-induced iNOS expression and NO production.
53	21450974	In contrast, inhibition of the ERK pathway using PD98059 dose dependently enhanced PGN-induced iNOS expression and NO production.
54	21450974	PGN-induced ERK activation was attenuated in ERK1/2 siRNA knocked-down macrophages; however, NO and iNOS expression were significantly enhanced.
55	21450974	An electrophoretic mobility shift assay showed that SP600125 inhibited PGN-induced NF-κB and AP-1 activation, whereas inhibition of the ERK pathway enhanced NF-κB activation, but with no effect on AP-1.
56	21450974	These results indicate that the JNK MAPK positively regulate PGN-induced iNOS and NO expression by activating NF-κB and AP-1 transcription factors, whereas the ERK pathway plays a negative regulatory role via affecting NF-κB activity.
57	21450974	The objectives of this study were to examine the roles of mitogen-activated protein kinases (MAPKs) and transcription factors (nuclear factor-κB [NF-κB] and activating protein 1 [AP-1]) in peptidoglycan (PGN)-induced iNOS expression and NO production in macrophages.
58	21450974	PGN stimulates the activation of all three classes of MAPKs, extracellular signal-related kinase (ERK), c-Jun N-terminal kinase (JNK), and p38(mapk) in macrophages, albeit with differential activation kinetics.
59	21450974	Using a selective inhibitor of JNK (SP600125) and JNK1/2 small interfering RNA (siRNA) knocked-down macrophages, it was observed that PGN-induced iNOS and NO expression is significantly inhibited.
60	21450974	This suggested that JNK MAPK plays an essential role in PGN-induced iNOS expression and NO production.
61	21450974	In contrast, inhibition of the ERK pathway using PD98059 dose dependently enhanced PGN-induced iNOS expression and NO production.
62	21450974	PGN-induced ERK activation was attenuated in ERK1/2 siRNA knocked-down macrophages; however, NO and iNOS expression were significantly enhanced.
63	21450974	An electrophoretic mobility shift assay showed that SP600125 inhibited PGN-induced NF-κB and AP-1 activation, whereas inhibition of the ERK pathway enhanced NF-κB activation, but with no effect on AP-1.
64	21450974	These results indicate that the JNK MAPK positively regulate PGN-induced iNOS and NO expression by activating NF-κB and AP-1 transcription factors, whereas the ERK pathway plays a negative regulatory role via affecting NF-κB activity.
65	23467931	Transcriptional profiling further supported the notion that the PGN- and Poly I:C-induced effects were mediated through binding to TLR2/nucleotide-binding oligomerization domain 2 and TLR3/MDA5, respectively.
66	24076409	Urease, BabA and SabA in the adhesion-step, PGN and LPS in the immune evasion-step, and CagA, VacA and Tipα in the mucosal damage-step were documented to play an important role in step-specific pathogenicity of H. pylori infection.
67	24076409	There is evidence further supporting a role of potentially functional polymorphisms of host genes directly responding to these pathogenic step-specific virulence factors in the susceptibility of gastric carcinogenesis, especially for urease-interacting HLA class II genes, BabA-interacting MUC1, PGN-interacting NOD1, LPS-interacting TLR4, and CagA-interacting PTPN11 and CDH1.
68	24076409	Urease, BabA and SabA in the adhesion-step, PGN and LPS in the immune evasion-step, and CagA, VacA and Tipα in the mucosal damage-step were documented to play an important role in step-specific pathogenicity of H. pylori infection.
69	24076409	There is evidence further supporting a role of potentially functional polymorphisms of host genes directly responding to these pathogenic step-specific virulence factors in the susceptibility of gastric carcinogenesis, especially for urease-interacting HLA class II genes, BabA-interacting MUC1, PGN-interacting NOD1, LPS-interacting TLR4, and CagA-interacting PTPN11 and CDH1.