Ignet

Gene Information

Gene symbol: IHH

Gene name: Indian hedgehog

HGNC ID: 5956

Synonyms: HHG2, BDA1

Related Genes

#	Gene Symbol	Number of hits
1	ACAN	1 hits
2	ADAMTSL3	1 hits
3	EFEMP1	1 hits
4	FGF2	1 hits
5	FGFR1	1 hits
6	FGFR3	1 hits
7	GNRH1	1 hits
8	GNRHR	1 hits
9	HHIP	1 hits
10	INS	1 hits
11	KAL1	1 hits
12	KISS1R	1 hits
13	LEP	1 hits
14	NELF	1 hits
15	NUDT6	1 hits
16	PDX1	1 hits
17	POR	1 hits
18	PTCH1	1 hits
19	PTH	1 hits
20	PTHLH	1 hits
21	SMO	1 hits

Related Sentences

#	PMID	Sentence
1	10861287	Increased expression of PATCHED: (PTC:) was observed, independent of unaltered expression of parathyroid hormone-related peptide (PTHrP) receptor and Indian Hedgehog (IHH:), suggesting a new regulatory role for Fgfr3 in embryos.
2	11181569	A Ser(365)-->Cys mutation of fibroblast growth factor receptor 3 in mouse downregulates Ihh/PTHrP signals and causes severe achondroplasia.
3	11181569	Missense mutations in fibroblast growth factor receptor 3 (FGFR3) result in several types of human skeletal dysplasia, including the neonatally lethal dwarfism known as thanatophoric dysplasia.
4	11181569	The receptor-activating mutation also resulted in downregulation of expression of the Indian hedgehog (IHH) and parathyroid hormone-related protein (PTHrP) receptor genes, both of which are important for bone growth.
5	11181569	Consistent with the in vivo observations, FGF2 inhibited bone growth in culture and induced downregulation of IHH and PTHrP receptor gene expression.
6	11181569	Furthermore, PTHrP partially reversed the inhibition of long bone growth caused by activation of FGFR3; however, it impaired the differentiation of chondrocytes in an FGFR3-independent manner.
7	11181569	A Ser(365)-->Cys mutation of fibroblast growth factor receptor 3 in mouse downregulates Ihh/PTHrP signals and causes severe achondroplasia.
8	11181569	Missense mutations in fibroblast growth factor receptor 3 (FGFR3) result in several types of human skeletal dysplasia, including the neonatally lethal dwarfism known as thanatophoric dysplasia.
9	11181569	The receptor-activating mutation also resulted in downregulation of expression of the Indian hedgehog (IHH) and parathyroid hormone-related protein (PTHrP) receptor genes, both of which are important for bone growth.
10	11181569	Consistent with the in vivo observations, FGF2 inhibited bone growth in culture and induced downregulation of IHH and PTHrP receptor gene expression.
11	11181569	Furthermore, PTHrP partially reversed the inhibition of long bone growth caused by activation of FGFR3; however, it impaired the differentiation of chondrocytes in an FGFR3-independent manner.
12	11181569	A Ser(365)-->Cys mutation of fibroblast growth factor receptor 3 in mouse downregulates Ihh/PTHrP signals and causes severe achondroplasia.
13	11181569	Missense mutations in fibroblast growth factor receptor 3 (FGFR3) result in several types of human skeletal dysplasia, including the neonatally lethal dwarfism known as thanatophoric dysplasia.
14	11181569	The receptor-activating mutation also resulted in downregulation of expression of the Indian hedgehog (IHH) and parathyroid hormone-related protein (PTHrP) receptor genes, both of which are important for bone growth.
15	11181569	Consistent with the in vivo observations, FGF2 inhibited bone growth in culture and induced downregulation of IHH and PTHrP receptor gene expression.
16	11181569	Furthermore, PTHrP partially reversed the inhibition of long bone growth caused by activation of FGFR3; however, it impaired the differentiation of chondrocytes in an FGFR3-independent manner.
17	12217324	Sonic Hedgehog (Shh) is a secreted morphogen that directs patterning and cellular differentiation through binding to its receptor Patched (Ptc).
18	12217324	Our results demonstrate that neither Shh nor Ihh is required for mammary gland morphogenesis and functional differentiation, suggesting that the two members of the Hedgehog family may have redundant function in activating the Ptc1 signaling pathway during mammary gland development.
19	12967338	Indian hedgehog (IHH) and its receptors patched (PTC) and smoothened (SMO) belong to the hedgehog family of signaling molecules, which are essential for a variety of patterning events during mammalian tIssue development.
20	12967338	IHH plays a role in pancreas organogenesis and differentiation, as well as in the regulation of insulin production.
21	12967338	Correlation between diabetic and non-diabetic CP patients revealed no significant difference in IHH, SMO, or PTC immunoreactivity.
22	12967338	Indian hedgehog (IHH) and its receptors patched (PTC) and smoothened (SMO) belong to the hedgehog family of signaling molecules, which are essential for a variety of patterning events during mammalian tIssue development.
23	12967338	IHH plays a role in pancreas organogenesis and differentiation, as well as in the regulation of insulin production.
24	12967338	Correlation between diabetic and non-diabetic CP patients revealed no significant difference in IHH, SMO, or PTC immunoreactivity.
25	12967338	Indian hedgehog (IHH) and its receptors patched (PTC) and smoothened (SMO) belong to the hedgehog family of signaling molecules, which are essential for a variety of patterning events during mammalian tIssue development.
26	12967338	IHH plays a role in pancreas organogenesis and differentiation, as well as in the regulation of insulin production.
27	12967338	Correlation between diabetic and non-diabetic CP patients revealed no significant difference in IHH, SMO, or PTC immunoreactivity.
28	15668393	At earlier stages, only a dorsal bud rudiment forms transiently and expresses the transcription factors Ipf1 and Hlxb9 but lacks the key transcription factor involved in the acquisition of a pancreatic fate, Ptf1a, as well as all endocrine precursor cells.
29	15668393	Regional specification of the gut also is perturbed in Tcf2-/- embryos as manifested by ectopic expression of Shh and lack of Ihh and Ipf1 in the posterior stomach and duodenum.
30	18183793	Leptin stimulates parathyroid hormone related peptide expression in the endochondral growth plate.
31	18183793	These three cell processes are known to be regulated by the interactions of parathyroid hormone-related peptide (PTHrP) and Indian hedgehog (Ihh) protein.
32	18183793	The aim of the present study was to examine the effect of leptin on the PTHrP/Ihh feedback loop.
33	18183793	Immunohistochemistry and in situ hybridization showed that in the pair-fed in vivo system as well as in the organ culture, leptin increased the level of PTHrP and reduced that of Ihh.
34	18183793	Leptin may affect chondrocyte proliferation and differentiation by activating the PTHrP/Ihh growth-restraining feedback loop in the postnatal growth plate.
35	18183793	Leptin stimulates parathyroid hormone related peptide expression in the endochondral growth plate.
36	18183793	These three cell processes are known to be regulated by the interactions of parathyroid hormone-related peptide (PTHrP) and Indian hedgehog (Ihh) protein.
37	18183793	The aim of the present study was to examine the effect of leptin on the PTHrP/Ihh feedback loop.
38	18183793	Immunohistochemistry and in situ hybridization showed that in the pair-fed in vivo system as well as in the organ culture, leptin increased the level of PTHrP and reduced that of Ihh.
39	18183793	Leptin may affect chondrocyte proliferation and differentiation by activating the PTHrP/Ihh growth-restraining feedback loop in the postnatal growth plate.
40	18183793	Leptin stimulates parathyroid hormone related peptide expression in the endochondral growth plate.
41	18183793	These three cell processes are known to be regulated by the interactions of parathyroid hormone-related peptide (PTHrP) and Indian hedgehog (Ihh) protein.
42	18183793	The aim of the present study was to examine the effect of leptin on the PTHrP/Ihh feedback loop.
43	18183793	Immunohistochemistry and in situ hybridization showed that in the pair-fed in vivo system as well as in the organ culture, leptin increased the level of PTHrP and reduced that of Ihh.
44	18183793	Leptin may affect chondrocyte proliferation and differentiation by activating the PTHrP/Ihh growth-restraining feedback loop in the postnatal growth plate.
45	18183793	Leptin stimulates parathyroid hormone related peptide expression in the endochondral growth plate.
46	18183793	These three cell processes are known to be regulated by the interactions of parathyroid hormone-related peptide (PTHrP) and Indian hedgehog (Ihh) protein.
47	18183793	The aim of the present study was to examine the effect of leptin on the PTHrP/Ihh feedback loop.
48	18183793	Immunohistochemistry and in situ hybridization showed that in the pair-fed in vivo system as well as in the organ culture, leptin increased the level of PTHrP and reduced that of Ihh.
49	18183793	Leptin may affect chondrocyte proliferation and differentiation by activating the PTHrP/Ihh growth-restraining feedback loop in the postnatal growth plate.
50	18391952	The loci we identified implicate genes in Hedgehog signaling (IHH, HHIP, PTCH1), extracellular matrix (EFEMP1, ADAMTSL3, ACAN) and cancer (CDK6, HMGA2, DLEU7) pathways, and provide new insights into human growth and developmental processes.
51	18463157	Idiopathic hypogonadotropic hypogonadism (IHH) and Kallmann syndrome (KS) are clinically and genetically heterogeneous disorders caused by a deficiency of gonadotrophin-releasing hormone (GnRH).
52	18463157	Mutations in three genes--KAL1, GNRHR and FGFR1--account for 15-20% of all causes of IHH/KS.
53	18463157	Fifty-four IHH/KS patients were studied for KAL1 deletions and 100 were studied for an autosomal panel of FGFR1, GNRH1, GNRHR, GPR54 and NELF gene deletions.
54	18463157	Our results indicate approximately 12% of KS males have KAL1 deletions, but intragenic deletions of the FGFR1, GNRH1, GNRHR, GPR54 and NELF genes are uncommon in IHH/KS.
55	18463157	Idiopathic hypogonadotropic hypogonadism (IHH) and Kallmann syndrome (KS) are clinically and genetically heterogeneous disorders caused by a deficiency of gonadotrophin-releasing hormone (GnRH).
56	18463157	Mutations in three genes--KAL1, GNRHR and FGFR1--account for 15-20% of all causes of IHH/KS.
57	18463157	Fifty-four IHH/KS patients were studied for KAL1 deletions and 100 were studied for an autosomal panel of FGFR1, GNRH1, GNRHR, GPR54 and NELF gene deletions.
58	18463157	Our results indicate approximately 12% of KS males have KAL1 deletions, but intragenic deletions of the FGFR1, GNRH1, GNRHR, GPR54 and NELF genes are uncommon in IHH/KS.
59	18463157	Idiopathic hypogonadotropic hypogonadism (IHH) and Kallmann syndrome (KS) are clinically and genetically heterogeneous disorders caused by a deficiency of gonadotrophin-releasing hormone (GnRH).
60	18463157	Mutations in three genes--KAL1, GNRHR and FGFR1--account for 15-20% of all causes of IHH/KS.
61	18463157	Fifty-four IHH/KS patients were studied for KAL1 deletions and 100 were studied for an autosomal panel of FGFR1, GNRH1, GNRHR, GPR54 and NELF gene deletions.
62	18463157	Our results indicate approximately 12% of KS males have KAL1 deletions, but intragenic deletions of the FGFR1, GNRH1, GNRHR, GPR54 and NELF genes are uncommon in IHH/KS.
63	18463157	Idiopathic hypogonadotropic hypogonadism (IHH) and Kallmann syndrome (KS) are clinically and genetically heterogeneous disorders caused by a deficiency of gonadotrophin-releasing hormone (GnRH).
64	18463157	Mutations in three genes--KAL1, GNRHR and FGFR1--account for 15-20% of all causes of IHH/KS.
65	18463157	Fifty-four IHH/KS patients were studied for KAL1 deletions and 100 were studied for an autosomal panel of FGFR1, GNRH1, GNRHR, GPR54 and NELF gene deletions.
66	18463157	Our results indicate approximately 12% of KS males have KAL1 deletions, but intragenic deletions of the FGFR1, GNRH1, GNRHR, GPR54 and NELF genes are uncommon in IHH/KS.
67	19264869	P450 oxidoreductase expressed in rat chondrocytes modulates chondrogenesis via cholesterol- and Indian Hedgehog-dependent mechanisms.
68	19264869	Cytochrome P450 oxidoreductase (POR) is the electron donor for microsomal cytochrome P450 enzymes and other non-P450 enzymes.
69	19264869	Because cholesterol is required for normal activity of the hedgehog proteins, we evaluated the effects of POR siRNAs on the expression of Indian hedgehog (Ihh), an important regulator of chondrogenesis.
70	19264869	POR siRNA-transfected chondrocytes exhibited reduced Ihh expression, with such effect being neutralized by cholesterol.
71	19264869	Lastly, recombinant human/mouse Ihh prevented the POR siRNA-mediated effects on chondrocyte proliferation, differentiation, and apoptosis.
72	19264869	Our findings suggest that the bone malformations associated with defective POR activity are due to reduced cholesterol synthesis and, in turn, reduced Ihh expression in chondrocytes.
73	19264869	P450 oxidoreductase expressed in rat chondrocytes modulates chondrogenesis via cholesterol- and Indian Hedgehog-dependent mechanisms.
74	19264869	Cytochrome P450 oxidoreductase (POR) is the electron donor for microsomal cytochrome P450 enzymes and other non-P450 enzymes.
75	19264869	Because cholesterol is required for normal activity of the hedgehog proteins, we evaluated the effects of POR siRNAs on the expression of Indian hedgehog (Ihh), an important regulator of chondrogenesis.
76	19264869	POR siRNA-transfected chondrocytes exhibited reduced Ihh expression, with such effect being neutralized by cholesterol.
77	19264869	Lastly, recombinant human/mouse Ihh prevented the POR siRNA-mediated effects on chondrocyte proliferation, differentiation, and apoptosis.
78	19264869	Our findings suggest that the bone malformations associated with defective POR activity are due to reduced cholesterol synthesis and, in turn, reduced Ihh expression in chondrocytes.
79	19264869	P450 oxidoreductase expressed in rat chondrocytes modulates chondrogenesis via cholesterol- and Indian Hedgehog-dependent mechanisms.
80	19264869	Cytochrome P450 oxidoreductase (POR) is the electron donor for microsomal cytochrome P450 enzymes and other non-P450 enzymes.
81	19264869	Because cholesterol is required for normal activity of the hedgehog proteins, we evaluated the effects of POR siRNAs on the expression of Indian hedgehog (Ihh), an important regulator of chondrogenesis.
82	19264869	POR siRNA-transfected chondrocytes exhibited reduced Ihh expression, with such effect being neutralized by cholesterol.
83	19264869	Lastly, recombinant human/mouse Ihh prevented the POR siRNA-mediated effects on chondrocyte proliferation, differentiation, and apoptosis.
84	19264869	Our findings suggest that the bone malformations associated with defective POR activity are due to reduced cholesterol synthesis and, in turn, reduced Ihh expression in chondrocytes.
85	19264869	P450 oxidoreductase expressed in rat chondrocytes modulates chondrogenesis via cholesterol- and Indian Hedgehog-dependent mechanisms.
86	19264869	Cytochrome P450 oxidoreductase (POR) is the electron donor for microsomal cytochrome P450 enzymes and other non-P450 enzymes.
87	19264869	Because cholesterol is required for normal activity of the hedgehog proteins, we evaluated the effects of POR siRNAs on the expression of Indian hedgehog (Ihh), an important regulator of chondrogenesis.
88	19264869	POR siRNA-transfected chondrocytes exhibited reduced Ihh expression, with such effect being neutralized by cholesterol.
89	19264869	Lastly, recombinant human/mouse Ihh prevented the POR siRNA-mediated effects on chondrocyte proliferation, differentiation, and apoptosis.
90	19264869	Our findings suggest that the bone malformations associated with defective POR activity are due to reduced cholesterol synthesis and, in turn, reduced Ihh expression in chondrocytes.