Ignet

Gene Information

Gene symbol: CCL16

Gene name: chemokine (C-C motif) ligand 16

HGNC ID: 10614

Synonyms: NCC-4, SCYL4, LEC, HCC-4, LMC, LCC-1, CKb12, Mtn-1

Related Genes

#	Gene Symbol	Number of hits
1	ARHGEF1	1 hits
2	IFNG	1 hits
3	NOS2A	1 hits
4	TNF	1 hits

Related Sentences

#	PMID	Sentence
1	20562522	Cell death of LSCs and LECs is essential for structural luteolysis.
2	20562522	We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI).
3	20562522	To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h.
4	20562522	The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05).
5	20562522	Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05).
6	20562522	Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG.
7	20562522	Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05).
8	20562522	In summary, TNF and IFNG increased cell death in cultured bovine LECs.
9	20562522	The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis.
10	20562522	Cell death of LSCs and LECs is essential for structural luteolysis.
11	20562522	We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI).
12	20562522	To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h.
13	20562522	The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05).
14	20562522	Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05).
15	20562522	Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG.
16	20562522	Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05).
17	20562522	In summary, TNF and IFNG increased cell death in cultured bovine LECs.
18	20562522	The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis.
19	20562522	Cell death of LSCs and LECs is essential for structural luteolysis.
20	20562522	We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI).
21	20562522	To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h.
22	20562522	The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05).
23	20562522	Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05).
24	20562522	Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG.
25	20562522	Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05).
26	20562522	In summary, TNF and IFNG increased cell death in cultured bovine LECs.
27	20562522	The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis.
28	22847916	The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs.
29	22847916	Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM).
30	22847916	NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05).
31	22847916	TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05).
32	22847916	TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05).
33	22847916	The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs.
34	22847916	P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs.
35	22847916	The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs.
36	22847916	Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM).
37	22847916	NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05).
38	22847916	TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05).
39	22847916	TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05).
40	22847916	The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs.
41	22847916	P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs.
42	22847916	The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs.
43	22847916	Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM).
44	22847916	NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05).
45	22847916	TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05).
46	22847916	TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05).
47	22847916	The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs.
48	22847916	P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs.
49	22847916	The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs.
50	22847916	Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM).
51	22847916	NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05).
52	22847916	TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05).
53	22847916	TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05).
54	22847916	The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs.
55	22847916	P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs.
56	22847916	The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs.
57	22847916	Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM).
58	22847916	NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05).
59	22847916	TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05).
60	22847916	TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05).
61	22847916	The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs.
62	22847916	P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs.