INT38503

Context Info Confidence 0.67 First Reported 1984 Last Reported 2009 Negated 0 Speculated 0 Reported most in Abstract Documents 11 Total Number 11 Disease Relevance 2.90 Pain Relevance 7.47

intracellular (Ripk2) kinase activity (Ripk2) cytoplasm (Ripk2)

Anatomy Link Frequency brain 2 gut 2 spinal cord 1 T cell 1 Ripk2 (Mus musculus)

Pain Link Frequency Relevance Heat Cholecystokinin 18 100.00 agonist 4 100.00 Endogenous opioid 2 99.36 narcan 19 99.02 Hyperalgesia 2 98.90 antinociception 11 98.86 allodynia 3 98.56 chemokine 17 98.44 tolerance 15 98.28 Kinase C 5 98.24

Disease Link Frequency Relevance Heat Diabetes Mellitus 34 99.14 Hyperalgesia 3 98.90 Neuropathic Pain 3 98.56 Multiple Sclerosis 57 96.80 Adhesions 2 93.44 Death 10 86.64 Lymphatic System Cancer 2 82.72 Apoptosis 11 70.68 Targeted Disruption 5 57.92 Autoimmune Disease 33 50.00

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Disease term

The results indicated that the reduction of endomorphin-2-induced antinociception in diabetic mice might be due, at least in part, to the activation of CCK(2) receptors.

Positive_regulation (activation) of CCK associated with antinociception and diabetes mellitus

1) Confidence 0.67 Published 2001 Journal Eur. J. Pharmacol. Section Abstract Doc Link 11282117 Disease Relevance 0.84 Pain Relevance 0.63

These results indicate that the thermal allodynia and hyperalgesia in diabetic mice may be due, at least in part, to the activation of CCK(B) receptors followed by the activation of PKC in the spinal cord.

Positive_regulation (activation) of CCK in spinal cord associated with kinase c, hyperalgesia, allodynia, diabetes mellitus and spinal cord

2) Confidence 0.67 Published 2001 Journal Brain Res. Section Abstract Doc Link 11172785 Disease Relevance 1.24 Pain Relevance 1.04

The results of the present study indicate that activation of both CCKB and CCKA receptors may prevent the development of tolerance to morphine, and the sulfate group in the CCK-8 molecule may be essential for the tolerance inhibition.

Positive_regulation (activation) of CCK associated with tolerance and morphine

3) Confidence 0.67 Published 1994 Journal Eur. J. Pharmacol. Section Abstract Doc Link 8206114 Disease Relevance 0 Pain Relevance 1.04

The antinociceptive activity of sulfated cholecystokinin octapeptide (CCK-8-S) was characterized by comparison with two other endogenous forms, unsulfated CCK-8 (CCK-8-U) and the carboxyl tetrapeptide fragment (CCK-4) and two other peptides present in the gut and brain: bombesin and neurotensin.

Positive_regulation (unsulfated) of CCK in brain associated with cholecystokinin and antinociceptive

4) Confidence 0.49 Published 1986 Journal Neuropharmacology Section Abstract Doc Link 3774112 Disease Relevance 0 Pain Relevance 0.35

The antinociceptive activity of sulfated cholecystokinin octapeptide (CCK-8-S) was characterized by comparison with two other endogenous forms, unsulfated CCK-8 (CCK-8-U) and the carboxyl tetrapeptide fragment (CCK-4) and two other peptides present in the gut and brain: bombesin and neurotensin.

Positive_regulation (unsulfated) of CCK in brain associated with cholecystokinin and antinociceptive

5) Confidence 0.49 Published 1986 Journal Neuropharmacology Section Abstract Doc Link 3774112 Disease Relevance 0 Pain Relevance 0.35

On the contrary, naloxone had no apparent effect on the insulin secretory response to the cholinergic agonist carbachol or the synthetic C-terminal octapeptide of cholecystokinin, CCK-8.

Positive_regulation (response) of CCK associated with agonist, narcan and cholecystokinin

6) Confidence 0.49 Published 1984 Journal Eur. J. Pharmacol. Section Abstract Doc Link 6090153 Disease Relevance 0 Pain Relevance 0.81

The results of the present study indicate that activation of both CCKB and CCKA receptors may prevent the development of tolerance to morphine, and the sulfate group in the CCK-8 molecule may be essential for the tolerance inhibition.

Positive_regulation (activation) of CCK associated with tolerance and morphine

7) Confidence 0.45 Published 1994 Journal Eur. J. Pharmacol. Section Abstract Doc Link 8206114 Disease Relevance 0 Pain Relevance 1.04

The top 30 differentially expressed genes in the non-T cell fraction included upregulation of cell division cycle 42 (CDC42), receptor-interacting serine/threonine kinase 2 (RIPK2), IL-1 receptor, type II (IL1R2), the chemokine MIP-2?

Positive_regulation (upregulation) of RIPK2 in T cell associated with chemokine

8) Confidence 0.21 Published 2009 Journal Mediators of Inflammation Section Body Doc Link PMC2768824 Disease Relevance 0.77 Pain Relevance 0.32

The antinociceptive activity of sulfated cholecystokinin octapeptide (CCK-8-S) was characterized by comparison with two other endogenous forms, unsulfated CCK-8 (CCK-8-U) and the carboxyl tetrapeptide fragment (CCK-4) and two other peptides present in the gut and brain: bombesin and neurotensin.

Positive_regulation (unsulfated) of CCK in gut associated with cholecystokinin and antinociceptive

9) Confidence 0.17 Published 1986 Journal Neuropharmacology Section Abstract Doc Link 3774112 Disease Relevance 0 Pain Relevance 0.35

The antinociceptive activity of sulfated cholecystokinin octapeptide (CCK-8-S) was characterized by comparison with two other endogenous forms, unsulfated CCK-8 (CCK-8-U) and the carboxyl tetrapeptide fragment (CCK-4) and two other peptides present in the gut and brain: bombesin and neurotensin.

Positive_regulation (unsulfated) of CCK in gut associated with cholecystokinin and antinociceptive

10) Confidence 0.17 Published 1986 Journal Neuropharmacology Section Abstract Doc Link 3774112 Disease Relevance 0 Pain Relevance 0.35

The existence of regulatory loops between both systems has been proposed, and the physiological antagonism between CCK, through activation of CCK2 receptors, and endogenous opioid systems has been demonstrated.

Positive_regulation (activation) of CCK2 associated with endogenous opioid and cholecystokinin

11) Confidence 0.16 Published 2003 Journal Drugs Today Section Abstract Doc Link 14702135 Disease Relevance 0.06 Pain Relevance 1.20

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