Ignet

Gene Information

Gene symbol: DLX5

Gene name: distal-less homeobox 5

HGNC ID: 2918

Related Genes

#	Gene Symbol	Number of hits
1	ACP5	1 hits
2	ADIPOQ	1 hits
3	ALPP	1 hits
4	BGLAP	1 hits
5	BMP2	1 hits
6	CD36	1 hits
7	COL1A1	1 hits
8	CTSK	1 hits
9	FGF2	1 hits
10	FOS	1 hits
11	GTF3A	1 hits
12	INS	1 hits
13	JUN	1 hits
14	MSX2	1 hits
15	RUNX2	1 hits
16	SP7	1 hits
17	TNFRSF11A	1 hits

Related Sentences

#	PMID	Sentence
1	9819228	Reciprocal regulation of osteocalcin transcription by the homeodomain proteins Msx2 and Dlx5.
2	9819228	Since the homeodomain proteins Dlx5 and Msx2 are both expressed by primary rat calvarial osteoblasts, we examined whether Msx2 and Dlx5 functionally interact to regulate the OC promoter.
3	9819228	In both primary rat calvarial and MC3T3E1 mouse calvarial osteoblasts, transient expression of Dlx5 only mildly augments basal OC promoter (luciferase reporter) activity, while Msx2 suppresses transcriptional activity by ca. 80%.
4	9819228	However, Dlx5 completely reverses Msx2 repression of the OC promoter.
5	9819228	Structure-function analyses using far-Western blot and transient cotransfection assays reveal that (i) Msx2 and Dlx5 can form dimers, (ii) Dlx5 residues 127-143 are necessary for dimerization and to reverse Msx2-dependent OC repression, and (iii) intrinsic DNA binding activity of Dlx5 is not required for OC regulation.
6	9819228	Dlx5 completely abrogates Msx2 suppression of OCFREB DNA binding activity, and residues required for Dlx5 transcriptional de-repression in vivo are also required for reversing inhibition of OCFREB binding in vitro.
7	9819228	Finally, Dlx5 reverses Msx2 inhibition of OC promoter activation by FGF2/forskolin.
8	9819228	Thus, Dlx5 regulates the expression of the OC promoter in calvarial osteoblasts in part by de-repression, antagonizing Msx2 repression of transcription factors that support basal OC promoter activity.
9	9819228	Reciprocal regulation of osteocalcin transcription by the homeodomain proteins Msx2 and Dlx5.
10	9819228	Since the homeodomain proteins Dlx5 and Msx2 are both expressed by primary rat calvarial osteoblasts, we examined whether Msx2 and Dlx5 functionally interact to regulate the OC promoter.
11	9819228	In both primary rat calvarial and MC3T3E1 mouse calvarial osteoblasts, transient expression of Dlx5 only mildly augments basal OC promoter (luciferase reporter) activity, while Msx2 suppresses transcriptional activity by ca. 80%.
12	9819228	However, Dlx5 completely reverses Msx2 repression of the OC promoter.
13	9819228	Structure-function analyses using far-Western blot and transient cotransfection assays reveal that (i) Msx2 and Dlx5 can form dimers, (ii) Dlx5 residues 127-143 are necessary for dimerization and to reverse Msx2-dependent OC repression, and (iii) intrinsic DNA binding activity of Dlx5 is not required for OC regulation.
14	9819228	Dlx5 completely abrogates Msx2 suppression of OCFREB DNA binding activity, and residues required for Dlx5 transcriptional de-repression in vivo are also required for reversing inhibition of OCFREB binding in vitro.
15	9819228	Finally, Dlx5 reverses Msx2 inhibition of OC promoter activation by FGF2/forskolin.
16	9819228	Thus, Dlx5 regulates the expression of the OC promoter in calvarial osteoblasts in part by de-repression, antagonizing Msx2 repression of transcription factors that support basal OC promoter activity.
17	9819228	Reciprocal regulation of osteocalcin transcription by the homeodomain proteins Msx2 and Dlx5.
18	9819228	Since the homeodomain proteins Dlx5 and Msx2 are both expressed by primary rat calvarial osteoblasts, we examined whether Msx2 and Dlx5 functionally interact to regulate the OC promoter.
19	9819228	In both primary rat calvarial and MC3T3E1 mouse calvarial osteoblasts, transient expression of Dlx5 only mildly augments basal OC promoter (luciferase reporter) activity, while Msx2 suppresses transcriptional activity by ca. 80%.
20	9819228	However, Dlx5 completely reverses Msx2 repression of the OC promoter.
21	9819228	Structure-function analyses using far-Western blot and transient cotransfection assays reveal that (i) Msx2 and Dlx5 can form dimers, (ii) Dlx5 residues 127-143 are necessary for dimerization and to reverse Msx2-dependent OC repression, and (iii) intrinsic DNA binding activity of Dlx5 is not required for OC regulation.
22	9819228	Dlx5 completely abrogates Msx2 suppression of OCFREB DNA binding activity, and residues required for Dlx5 transcriptional de-repression in vivo are also required for reversing inhibition of OCFREB binding in vitro.
23	9819228	Finally, Dlx5 reverses Msx2 inhibition of OC promoter activation by FGF2/forskolin.
24	9819228	Thus, Dlx5 regulates the expression of the OC promoter in calvarial osteoblasts in part by de-repression, antagonizing Msx2 repression of transcription factors that support basal OC promoter activity.
25	9819228	Reciprocal regulation of osteocalcin transcription by the homeodomain proteins Msx2 and Dlx5.
26	9819228	Since the homeodomain proteins Dlx5 and Msx2 are both expressed by primary rat calvarial osteoblasts, we examined whether Msx2 and Dlx5 functionally interact to regulate the OC promoter.
27	9819228	In both primary rat calvarial and MC3T3E1 mouse calvarial osteoblasts, transient expression of Dlx5 only mildly augments basal OC promoter (luciferase reporter) activity, while Msx2 suppresses transcriptional activity by ca. 80%.
28	9819228	However, Dlx5 completely reverses Msx2 repression of the OC promoter.
29	9819228	Structure-function analyses using far-Western blot and transient cotransfection assays reveal that (i) Msx2 and Dlx5 can form dimers, (ii) Dlx5 residues 127-143 are necessary for dimerization and to reverse Msx2-dependent OC repression, and (iii) intrinsic DNA binding activity of Dlx5 is not required for OC regulation.
30	9819228	Dlx5 completely abrogates Msx2 suppression of OCFREB DNA binding activity, and residues required for Dlx5 transcriptional de-repression in vivo are also required for reversing inhibition of OCFREB binding in vitro.
31	9819228	Finally, Dlx5 reverses Msx2 inhibition of OC promoter activation by FGF2/forskolin.
32	9819228	Thus, Dlx5 regulates the expression of the OC promoter in calvarial osteoblasts in part by de-repression, antagonizing Msx2 repression of transcription factors that support basal OC promoter activity.
33	9819228	Reciprocal regulation of osteocalcin transcription by the homeodomain proteins Msx2 and Dlx5.
34	9819228	Since the homeodomain proteins Dlx5 and Msx2 are both expressed by primary rat calvarial osteoblasts, we examined whether Msx2 and Dlx5 functionally interact to regulate the OC promoter.
35	9819228	In both primary rat calvarial and MC3T3E1 mouse calvarial osteoblasts, transient expression of Dlx5 only mildly augments basal OC promoter (luciferase reporter) activity, while Msx2 suppresses transcriptional activity by ca. 80%.
36	9819228	However, Dlx5 completely reverses Msx2 repression of the OC promoter.
37	9819228	Structure-function analyses using far-Western blot and transient cotransfection assays reveal that (i) Msx2 and Dlx5 can form dimers, (ii) Dlx5 residues 127-143 are necessary for dimerization and to reverse Msx2-dependent OC repression, and (iii) intrinsic DNA binding activity of Dlx5 is not required for OC regulation.
38	9819228	Dlx5 completely abrogates Msx2 suppression of OCFREB DNA binding activity, and residues required for Dlx5 transcriptional de-repression in vivo are also required for reversing inhibition of OCFREB binding in vitro.
39	9819228	Finally, Dlx5 reverses Msx2 inhibition of OC promoter activation by FGF2/forskolin.
40	9819228	Thus, Dlx5 regulates the expression of the OC promoter in calvarial osteoblasts in part by de-repression, antagonizing Msx2 repression of transcription factors that support basal OC promoter activity.
41	9819228	Reciprocal regulation of osteocalcin transcription by the homeodomain proteins Msx2 and Dlx5.
42	9819228	Since the homeodomain proteins Dlx5 and Msx2 are both expressed by primary rat calvarial osteoblasts, we examined whether Msx2 and Dlx5 functionally interact to regulate the OC promoter.
43	9819228	In both primary rat calvarial and MC3T3E1 mouse calvarial osteoblasts, transient expression of Dlx5 only mildly augments basal OC promoter (luciferase reporter) activity, while Msx2 suppresses transcriptional activity by ca. 80%.
44	9819228	However, Dlx5 completely reverses Msx2 repression of the OC promoter.
45	9819228	Structure-function analyses using far-Western blot and transient cotransfection assays reveal that (i) Msx2 and Dlx5 can form dimers, (ii) Dlx5 residues 127-143 are necessary for dimerization and to reverse Msx2-dependent OC repression, and (iii) intrinsic DNA binding activity of Dlx5 is not required for OC regulation.
46	9819228	Dlx5 completely abrogates Msx2 suppression of OCFREB DNA binding activity, and residues required for Dlx5 transcriptional de-repression in vivo are also required for reversing inhibition of OCFREB binding in vitro.
47	9819228	Finally, Dlx5 reverses Msx2 inhibition of OC promoter activation by FGF2/forskolin.
48	9819228	Thus, Dlx5 regulates the expression of the OC promoter in calvarial osteoblasts in part by de-repression, antagonizing Msx2 repression of transcription factors that support basal OC promoter activity.
49	9819228	Reciprocal regulation of osteocalcin transcription by the homeodomain proteins Msx2 and Dlx5.
50	9819228	Since the homeodomain proteins Dlx5 and Msx2 are both expressed by primary rat calvarial osteoblasts, we examined whether Msx2 and Dlx5 functionally interact to regulate the OC promoter.
51	9819228	In both primary rat calvarial and MC3T3E1 mouse calvarial osteoblasts, transient expression of Dlx5 only mildly augments basal OC promoter (luciferase reporter) activity, while Msx2 suppresses transcriptional activity by ca. 80%.
52	9819228	However, Dlx5 completely reverses Msx2 repression of the OC promoter.
53	9819228	Structure-function analyses using far-Western blot and transient cotransfection assays reveal that (i) Msx2 and Dlx5 can form dimers, (ii) Dlx5 residues 127-143 are necessary for dimerization and to reverse Msx2-dependent OC repression, and (iii) intrinsic DNA binding activity of Dlx5 is not required for OC regulation.
54	9819228	Dlx5 completely abrogates Msx2 suppression of OCFREB DNA binding activity, and residues required for Dlx5 transcriptional de-repression in vivo are also required for reversing inhibition of OCFREB binding in vitro.
55	9819228	Finally, Dlx5 reverses Msx2 inhibition of OC promoter activation by FGF2/forskolin.
56	9819228	Thus, Dlx5 regulates the expression of the OC promoter in calvarial osteoblasts in part by de-repression, antagonizing Msx2 repression of transcription factors that support basal OC promoter activity.
57	9819228	Reciprocal regulation of osteocalcin transcription by the homeodomain proteins Msx2 and Dlx5.
58	9819228	Since the homeodomain proteins Dlx5 and Msx2 are both expressed by primary rat calvarial osteoblasts, we examined whether Msx2 and Dlx5 functionally interact to regulate the OC promoter.
59	9819228	In both primary rat calvarial and MC3T3E1 mouse calvarial osteoblasts, transient expression of Dlx5 only mildly augments basal OC promoter (luciferase reporter) activity, while Msx2 suppresses transcriptional activity by ca. 80%.
60	9819228	However, Dlx5 completely reverses Msx2 repression of the OC promoter.
61	9819228	Structure-function analyses using far-Western blot and transient cotransfection assays reveal that (i) Msx2 and Dlx5 can form dimers, (ii) Dlx5 residues 127-143 are necessary for dimerization and to reverse Msx2-dependent OC repression, and (iii) intrinsic DNA binding activity of Dlx5 is not required for OC regulation.
62	9819228	Dlx5 completely abrogates Msx2 suppression of OCFREB DNA binding activity, and residues required for Dlx5 transcriptional de-repression in vivo are also required for reversing inhibition of OCFREB binding in vitro.
63	9819228	Finally, Dlx5 reverses Msx2 inhibition of OC promoter activation by FGF2/forskolin.
64	9819228	Thus, Dlx5 regulates the expression of the OC promoter in calvarial osteoblasts in part by de-repression, antagonizing Msx2 repression of transcription factors that support basal OC promoter activity.
65	12488363	This deficit was evident at the molecular level as shown by diminished expression of osteocalcin, collagen types I.
66	12488363	When transcription factors were examined, core-binding factor alpha1 (Cbfa1)/runt domain factor-2 (Runx-2) and human homolog of the drosophila distal-less gene (Dlx5) expression were substantially reduced in the diabetic, compared with control, groups on d 4 and 6.
67	12488363	C-fos but not c-jun expression was also suppressed in the diabetic group but not closely linked to bone formation.
68	12488363	Insulin treatment substantially reversed the effect of diabetes on the expression of bone matrix osteocalcin and collagen type I and transcription factors Cbfa1/Runx2 and Dlx5.
69	12488363	These results indicate that diabetic animals produce sufficient amounts of immature mesenchymal tissue but fail to adequately express genes that regulate osteoblast differentiation, Cbfa1/Runx-2 and Dlx5, which in turn, leads to decreased bone formation.
70	12488363	This deficit was evident at the molecular level as shown by diminished expression of osteocalcin, collagen types I.
71	12488363	When transcription factors were examined, core-binding factor alpha1 (Cbfa1)/runt domain factor-2 (Runx-2) and human homolog of the drosophila distal-less gene (Dlx5) expression were substantially reduced in the diabetic, compared with control, groups on d 4 and 6.
72	12488363	C-fos but not c-jun expression was also suppressed in the diabetic group but not closely linked to bone formation.
73	12488363	Insulin treatment substantially reversed the effect of diabetes on the expression of bone matrix osteocalcin and collagen type I and transcription factors Cbfa1/Runx2 and Dlx5.
74	12488363	These results indicate that diabetic animals produce sufficient amounts of immature mesenchymal tissue but fail to adequately express genes that regulate osteoblast differentiation, Cbfa1/Runx-2 and Dlx5, which in turn, leads to decreased bone formation.
75	12488363	This deficit was evident at the molecular level as shown by diminished expression of osteocalcin, collagen types I.
76	12488363	When transcription factors were examined, core-binding factor alpha1 (Cbfa1)/runt domain factor-2 (Runx-2) and human homolog of the drosophila distal-less gene (Dlx5) expression were substantially reduced in the diabetic, compared with control, groups on d 4 and 6.
77	12488363	C-fos but not c-jun expression was also suppressed in the diabetic group but not closely linked to bone formation.
78	12488363	Insulin treatment substantially reversed the effect of diabetes on the expression of bone matrix osteocalcin and collagen type I and transcription factors Cbfa1/Runx2 and Dlx5.
79	12488363	These results indicate that diabetic animals produce sufficient amounts of immature mesenchymal tissue but fail to adequately express genes that regulate osteoblast differentiation, Cbfa1/Runx-2 and Dlx5, which in turn, leads to decreased bone formation.
80	14500573	This compound improves insulin sensitivity through the activation of the nuclear receptor, peroxisome proliferator-activated receptor-gamma (PPAR-gamma).
81	14500573	In addition to sensitizing cells to insulin, the PPAR-gamma2 isoform appears to be critical for the regulation of osteoblast and adipocyte differentiation from common mesenchymal bone marrow progenitors.
82	14500573	We have demonstrated previously that PPAR-gamma2 activated with rosiglitazone acts as a dominant inhibitor of osteoblastogenesis in murine bone marrow in vitro.
83	14500573	Changes in bone morphology and structure were accompanied by changes in the expression of osteoblast- and adipocyte-specific marker genes; the expression of the osteoblast-specific genes Runx2/Cbfa1, Dlx5, and alpha1(I)collagen were decreased, whereas the expression of the adipocyte-specific fatty acid binding protein aP2, was increased.
84	20818503	Increased expression of the receptor for activation of NF-kappaB and decreased runt-related transcription factor 2 expression in bone of rats with streptozotocin-induced diabetes.
85	20818503	Insulin-dependent diabetes mellitus (IDDM) is associated with an increased risk of osteopenia/osteoporosis in humans.
86	20818503	Markers of bone formation, alkaline phosphatase (ALP) activity and the number of osteoblasts in the proximal tibia and the serum osteocalcin level, were significantly lower.
87	20818503	Markers of bone resorption, activity of tartrate-resistant acid phosphatase (TRAP) and cathepsin K and the number of osteoclasts in the proximal tibia and urinary excretion of deoxypyridinoline, were higher in diabetic rats than control rats. mRNA levels of receptor for activation of NF-kappaB (RANK), c-fos, c-jun, TRAP and cathepsin K were significantly increased in diabetic rats, although RANK ligand, osteoprotegerin, macrophage colony-stimulating factor and c-fms levels were similar to the control value.
88	20818503	The decreased expression of ALP, osteoclacin and collagen mRNA in diabetic rats was associated with decreases in the expression of Runx2, Dlx5 and osterix and an unaltered expression of bone morphogenic protein-2.
89	20818503	The level of RANK protein increased and Runx2 protein decreased in diabetic rats.
90	20818503	These suggested that short-term IDDM induced upregulation of osteoclastogenesis with an increase in RANK and downregulation of osteoblastogenesis with a decrease in Runx2 in bone.
91	21567076	Insulin-dependent diabetes mellitus decreases osteoblastogenesis associated with the inhibition of Wnt signaling through increased expression of Sost and Dkk1 and inhibition of Akt activation.
92	21567076	Insulin-dependent diabetes mellitus (IDDM) is known to be associated with an increased risk of osteopenia.
93	21567076	After 4 weeks, the diabetic rats exhibited bone loss, low levels of osteocalcin, insulin-like growth factor-I (IGF-I) and bone alkaline phosphatase (ALP) activity with normal levels of bone tartrate-resistant acid phosphatase (TRAP) and cathepsin K activity, and urinary excretion of deoxypyridinoline (Dpd).
94	21567076	The decreased expression of ALP, osteoclacin and collagen mRNA was associated with a decrease in the expression of runt-related transcription factor 2 (Runx2), Osterix and distal-less homeobox 5 (Dlx5) and an unaltered expression of bone morphogenic protein-2 (BMP2).
95	21567076	The protein levels of Runx2, phosphorylated glycogen synthase kinase 3β (GSK3β), active β-catenin and β-catenin decreased.
96	21567076	The mRNA and protein levels of sclerosteosis (Sost) and Dickkopf 1 (Dkk1), inhibitors of Wnt signaling, increased.
97	21567076	The mRNA expression of IGF-I and the IGF-I receptor (IGF-IR) was suppressed.
98	21567076	These changes observed in the bone of diabetic rats were reversed by treatment with insulin, but not by normalization of the circulating IGF-I levels by treatment with IGF-I.
99	21567076	These results suggest that insulin-deficiency in IDDM decreases osteoblastogenesis associated with inhibition of Wnt signaling through the increased expression of Sost and Dkk1 and the inhibition of Akt activation.
100	23735664	The Zn supplement prevented a decrease in the activity and mRNA of alkaline phosphatase (ALP), osteocalcin mRNA, and hydroxyproline and calcium levels, and an increase in the activity and mRNA of tartrate-resistant acid phosphatase (TRAP) and cathepsin K in the proximal tibia of diabetic rats.
101	23735664	The increase in mRNA levels of receptor for activation of NF-κB (RANK), c-fos, c-jun, TRAP, and cathepsin K and decrease in the expression of Runx2, Dlx5, osterix, ALP, osteocalcin, and collagen were prevented by the supplement.
102	23735664	The decrease in β-catenin, phosphorylated GSK3β, phosphorylated Akt, insulin-like growth factor 1 (IGF-1), and IGF-1 receptor (IGF-1R) protein levels in diabetic rats was also inhibited, although Zn did not affect the diabetes-increased gene and protein expression of Sost and Dkk1.
103	23735664	These results suggested that Zn prevented the diabetes-induced increase in osteoclastogenesis and decrease in osteoblastogenesis by inhibiting RANK expression and stimulating IGF-1/IGF-1R/Akt/GSK3β/β-catenin signaling, respectively.