Ignet

Gene Information

Gene symbol: POMC

Gene name: proopiomelanocortin

HGNC ID: 9201

Synonyms: MSH, POC, CLIP, ACTH, NPP, LPH

Related Genes

#	Gene Symbol	Number of hits
1	AVP	1 hits
2	B3GAT1	1 hits
3	CD28	1 hits
4	CRH	1 hits
5	GHRL	1 hits
6	IL10	1 hits
7	IL2	1 hits
8	IL6	1 hits
9	INS	1 hits
10	NPS	1 hits
11	NPY	1 hits
12	PRL	1 hits
13	TAC1	1 hits
14	TNF	1 hits

Related Sentences

#	PMID	Sentence
1	1693118	Corticotropin releasing hormone and arginine vasopressin stimulation of ACTH and substance P in human mononuclear leukocytes.
2	1693118	Bacterial lipopolysaccharide (LPS) and corticotropin releasing hormone (CRH) plus arginine vasopressin (AVP) induce immunoassayable (1-13)ACTH (alpha MSH) from mononuclear leukocytes.
3	1693118	We studied the ability of LPS and CRH + AVP to in vitro stimulate native ACTH (not alpha MSH) and substance P (SP) production and thymidine incorporation in human mononuclear leukocytes.
4	1693118	Neither CRH + AVP nor LPS stimulated detectable amounts of intracellular or extracellular ACTH (less than 15 pg/8 x 10(6) cells or total medium) or SP (less than 50 pg/8 x 10(6) cells or total medium) at 1, 2, 3 or 4 days of incubation.
5	1693118	Corticotropin releasing hormone and arginine vasopressin stimulation of ACTH and substance P in human mononuclear leukocytes.
6	1693118	Bacterial lipopolysaccharide (LPS) and corticotropin releasing hormone (CRH) plus arginine vasopressin (AVP) induce immunoassayable (1-13)ACTH (alpha MSH) from mononuclear leukocytes.
7	1693118	We studied the ability of LPS and CRH + AVP to in vitro stimulate native ACTH (not alpha MSH) and substance P (SP) production and thymidine incorporation in human mononuclear leukocytes.
8	1693118	Neither CRH + AVP nor LPS stimulated detectable amounts of intracellular or extracellular ACTH (less than 15 pg/8 x 10(6) cells or total medium) or SP (less than 50 pg/8 x 10(6) cells or total medium) at 1, 2, 3 or 4 days of incubation.
9	1693118	Corticotropin releasing hormone and arginine vasopressin stimulation of ACTH and substance P in human mononuclear leukocytes.
10	1693118	Bacterial lipopolysaccharide (LPS) and corticotropin releasing hormone (CRH) plus arginine vasopressin (AVP) induce immunoassayable (1-13)ACTH (alpha MSH) from mononuclear leukocytes.
11	1693118	We studied the ability of LPS and CRH + AVP to in vitro stimulate native ACTH (not alpha MSH) and substance P (SP) production and thymidine incorporation in human mononuclear leukocytes.
12	1693118	Neither CRH + AVP nor LPS stimulated detectable amounts of intracellular or extracellular ACTH (less than 15 pg/8 x 10(6) cells or total medium) or SP (less than 50 pg/8 x 10(6) cells or total medium) at 1, 2, 3 or 4 days of incubation.
13	1693118	Corticotropin releasing hormone and arginine vasopressin stimulation of ACTH and substance P in human mononuclear leukocytes.
14	1693118	Bacterial lipopolysaccharide (LPS) and corticotropin releasing hormone (CRH) plus arginine vasopressin (AVP) induce immunoassayable (1-13)ACTH (alpha MSH) from mononuclear leukocytes.
15	1693118	We studied the ability of LPS and CRH + AVP to in vitro stimulate native ACTH (not alpha MSH) and substance P (SP) production and thymidine incorporation in human mononuclear leukocytes.
16	1693118	Neither CRH + AVP nor LPS stimulated detectable amounts of intracellular or extracellular ACTH (less than 15 pg/8 x 10(6) cells or total medium) or SP (less than 50 pg/8 x 10(6) cells or total medium) at 1, 2, 3 or 4 days of incubation.
17	1706244	Hormonal parameters such as TSH, PRL, ACTH, progesterone, cortisol, T3 and T4 were measured by RIA in sera in control pre-vaccine cycles as well as at 3, 6, and 12 months after primary vaccine immunization.
18	2239430	This monokine has now been shown to activate the release of ACTH by a hypothalamic mechanism with release of CRF and possibly vasopressin, which stimulates the corticotrophs.
19	2239430	We have found that this monokine can act following its third ventricular injection to stimulate ACTH, PRL, and GH release and to inhibit TSH release, at least in part, by release of prostaglandins since indomethacin, an inhibitor of prostaglandin synthesis, produced a blockade of the responses except for those of ACTH.
20	2239430	This monokine has now been shown to activate the release of ACTH by a hypothalamic mechanism with release of CRF and possibly vasopressin, which stimulates the corticotrophs.
21	2239430	We have found that this monokine can act following its third ventricular injection to stimulate ACTH, PRL, and GH release and to inhibit TSH release, at least in part, by release of prostaglandins since indomethacin, an inhibitor of prostaglandin synthesis, produced a blockade of the responses except for those of ACTH.
22	2247306	Frequent regression of tumors and subjective improvement by vaccine therapy of patients may be explained by: a) infection of tumor cells by the virus and so enhancing their immunogenicity, b) activation of cells of the immune system, increased production of interferons, tumor necrosis factor-alpha and other cytokines, c) increased production of ACTH and beta endorphin by monocytes and lymphocytes resulting in an improvement in the general well-being.
23	2430992	In vitro studies with human leukocytes from normal subjects incubated with ACTH, insulin, or typhoid vaccine were also performed.
24	2430992	Patients with normal pituitary ACTH production had an increase in the number of ACTH immunofluorescence-positive cells 1 h after insulin administration [25 +/- 5% (+/- SEM) to 44 +/- 6% P less than 0.05], and no change after typhoid administration.
25	2430992	ACTH-deficient patients had no change after insulin administration and a significant rise 6 h after typhoid vaccine treatment (24 +/- 12% to 50 +/- 6%; P less than 0.05).
26	2430992	The number of ACTH immunofluorescence-positive cells did not increase when mononuclear leukocytes were incubated in vitro with ACTH or insulin (with or without glucose deprivation).
27	2430992	These data suggest that the number of human mononuclear leukocytes containing immunoreactive ACTH is increased by at least 2 stimuli: 1) a central factor(s), such as CRH, accounting for the in vivo rise 1 h after insulin administration in patients with an intact hypothalamic-pituitary axis, and 2) an interferon inducer (e.g. typhoid antigen), accounting for the typhoid antigen-induced rise in the number of ACTH-positive cells in vivo in ACTH-deficient patients and in vitro.
28	2430992	In vitro studies with human leukocytes from normal subjects incubated with ACTH, insulin, or typhoid vaccine were also performed.
29	2430992	Patients with normal pituitary ACTH production had an increase in the number of ACTH immunofluorescence-positive cells 1 h after insulin administration [25 +/- 5% (+/- SEM) to 44 +/- 6% P less than 0.05], and no change after typhoid administration.
30	2430992	ACTH-deficient patients had no change after insulin administration and a significant rise 6 h after typhoid vaccine treatment (24 +/- 12% to 50 +/- 6%; P less than 0.05).
31	2430992	The number of ACTH immunofluorescence-positive cells did not increase when mononuclear leukocytes were incubated in vitro with ACTH or insulin (with or without glucose deprivation).
32	2430992	These data suggest that the number of human mononuclear leukocytes containing immunoreactive ACTH is increased by at least 2 stimuli: 1) a central factor(s), such as CRH, accounting for the in vivo rise 1 h after insulin administration in patients with an intact hypothalamic-pituitary axis, and 2) an interferon inducer (e.g. typhoid antigen), accounting for the typhoid antigen-induced rise in the number of ACTH-positive cells in vivo in ACTH-deficient patients and in vitro.
33	2430992	In vitro studies with human leukocytes from normal subjects incubated with ACTH, insulin, or typhoid vaccine were also performed.
34	2430992	Patients with normal pituitary ACTH production had an increase in the number of ACTH immunofluorescence-positive cells 1 h after insulin administration [25 +/- 5% (+/- SEM) to 44 +/- 6% P less than 0.05], and no change after typhoid administration.
35	2430992	ACTH-deficient patients had no change after insulin administration and a significant rise 6 h after typhoid vaccine treatment (24 +/- 12% to 50 +/- 6%; P less than 0.05).
36	2430992	The number of ACTH immunofluorescence-positive cells did not increase when mononuclear leukocytes were incubated in vitro with ACTH or insulin (with or without glucose deprivation).
37	2430992	These data suggest that the number of human mononuclear leukocytes containing immunoreactive ACTH is increased by at least 2 stimuli: 1) a central factor(s), such as CRH, accounting for the in vivo rise 1 h after insulin administration in patients with an intact hypothalamic-pituitary axis, and 2) an interferon inducer (e.g. typhoid antigen), accounting for the typhoid antigen-induced rise in the number of ACTH-positive cells in vivo in ACTH-deficient patients and in vitro.
38	2430992	In vitro studies with human leukocytes from normal subjects incubated with ACTH, insulin, or typhoid vaccine were also performed.
39	2430992	Patients with normal pituitary ACTH production had an increase in the number of ACTH immunofluorescence-positive cells 1 h after insulin administration [25 +/- 5% (+/- SEM) to 44 +/- 6% P less than 0.05], and no change after typhoid administration.
40	2430992	ACTH-deficient patients had no change after insulin administration and a significant rise 6 h after typhoid vaccine treatment (24 +/- 12% to 50 +/- 6%; P less than 0.05).
41	2430992	The number of ACTH immunofluorescence-positive cells did not increase when mononuclear leukocytes were incubated in vitro with ACTH or insulin (with or without glucose deprivation).
42	2430992	These data suggest that the number of human mononuclear leukocytes containing immunoreactive ACTH is increased by at least 2 stimuli: 1) a central factor(s), such as CRH, accounting for the in vivo rise 1 h after insulin administration in patients with an intact hypothalamic-pituitary axis, and 2) an interferon inducer (e.g. typhoid antigen), accounting for the typhoid antigen-induced rise in the number of ACTH-positive cells in vivo in ACTH-deficient patients and in vitro.
43	2430992	In vitro studies with human leukocytes from normal subjects incubated with ACTH, insulin, or typhoid vaccine were also performed.
44	2430992	Patients with normal pituitary ACTH production had an increase in the number of ACTH immunofluorescence-positive cells 1 h after insulin administration [25 +/- 5% (+/- SEM) to 44 +/- 6% P less than 0.05], and no change after typhoid administration.
45	2430992	ACTH-deficient patients had no change after insulin administration and a significant rise 6 h after typhoid vaccine treatment (24 +/- 12% to 50 +/- 6%; P less than 0.05).
46	2430992	The number of ACTH immunofluorescence-positive cells did not increase when mononuclear leukocytes were incubated in vitro with ACTH or insulin (with or without glucose deprivation).
47	2430992	These data suggest that the number of human mononuclear leukocytes containing immunoreactive ACTH is increased by at least 2 stimuli: 1) a central factor(s), such as CRH, accounting for the in vivo rise 1 h after insulin administration in patients with an intact hypothalamic-pituitary axis, and 2) an interferon inducer (e.g. typhoid antigen), accounting for the typhoid antigen-induced rise in the number of ACTH-positive cells in vivo in ACTH-deficient patients and in vitro.
48	7522168	Response of interleukin-6-deficient mice to tumor necrosis factor-induced metabolic changes and lethality.
49	7522168	Whether interleukin (IL)-6 contributes to tumor necrosis factor (TNF)-induced lethal shock or whether, on the contrary, it is part of a protective feedback system, remains unresolved.
50	7522168	We have tested the susceptibility of these to TNF-induced metabolic changes and lethality in different models, and compared the results with those obtained with IL-6+/+ wild-type mice.
51	7522168	Furthermore, IL-6(0/0) mice could be equally well desensitized (by IL-1) to TNF/GalN-induced lethality and tolerized to TNF-induced shock as IL-6+/+ mice.
52	7522168	We also observed that, in response to turpentine, TNF or IL-1, IL-6(0/0) mice produced significantly less acute phase proteins (APP) than IL-6+/+ mice.
53	7522168	In IL-6(0/0) mice, less corticosterone was induced by TNF than in the control mice, while the response to adrenocorticotropic hormone was the same.
54	7522168	The results indicate that IL-6 is not contributing in a major way to the pathogenesis leading to TNF-induced shock, and that neither IL-6 nor the APP studied are essential for a protective feedback system.
55	8270123	Prior to immunization, at approximately 1 year of age, cardiovascular parameters, and several plasma parameters [cortisol, adrenocorticotrophic hormone (ACTH), growth hormone (GH), interleukin-2 (IL-2), and total plasma immunoglobulin G (IgG)] were measured during a brief period of captivity.
56	8270123	Levels of plasma cortisol, ACTH, total IgG, and IL-2 noted at the time of capture were unrelated to subsequent antibody levels.
57	8270123	Prior to immunization, at approximately 1 year of age, cardiovascular parameters, and several plasma parameters [cortisol, adrenocorticotrophic hormone (ACTH), growth hormone (GH), interleukin-2 (IL-2), and total plasma immunoglobulin G (IgG)] were measured during a brief period of captivity.
58	8270123	Levels of plasma cortisol, ACTH, total IgG, and IL-2 noted at the time of capture were unrelated to subsequent antibody levels.
59	12642031	In contrast, no-difference was observed in anti-Vpr IgG between NP-S and NP-P, although both were significantly higher than FPs (P </= 0.001).
60	12922116	The anti-hemagglutinins (HI), tumour necrosis factor alpha (TNFalpha), interleukin (IL) 1beta, IL6, IL10, ACTH/cortisol axis, anti-CMV antibodies and CD28+CD57- lymphocytes were assessed.
61	12922116	Non-responders of both ages we characterised by higher levels of anti-CMV IgG and higher percentages of CD57+CD28- lymphocytes (known to be associated with CMV carrier status) together with increased concentrations of TNFalpha and IL6 and decreased levels of cortisol.
62	12922116	The anti-influenza vaccine induced increase in TNFalpha and IL10 in the all non-responders, while cortisol increased only in the young.
63	16846451	The serum concentration of neuroendocrine parameters [prolactin, cortisol, adrenocorticotropic hormone (ACTH)] was also measured after 6 months of therapy.
64	25555181	The ghrelin receptor, growth-hormone secretagogue receptor type 1a, is able to bind acylated ghrelin.
65	25555181	Moreover, by acting on vagal afferents or centrally, ghrelin can activate hypothalamic arcuate neurons that secrete the orexigenic peptides neuropeptide Y and agouti-related peptide, and inhibit the anorexigenic neurons secreting pro-opiomelanocortin and α-melanocyte-stimulating hormone.