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Pathways

PathWhiz ID Pathway Meta Data

PW064735

Pw064735 View Pathway
metabolic

TLR4-IL-1 IRAK pathway

Homo sapiens

PW064786

Pw064786 View Pathway
physiological

tnf

Mus musculus

PW101526

Pw101526 View Pathway
signaling

TNF/Stress Related Signaling

Rattus norvegicus
Tumour necrosis factor alpha (TNF-a) is a cytokine that activates TNF rector 1 (TNFR1) signalling complex. TNFR1 mediates cell death signalling and inflammation in response to cytokines, bacteria and cellular stress. The classical NFkB pathway involves activation of TNF receptor associated factor 2, receptor interacting serine/threonine protein kinase and death domains which activate the IKK complex, phosphorylating the IKB proteins triggering their degradation resulting in NF-kB dimers dissociation and release. Caspase 2 interacts with TNF-receptor associated factor 2 and receptor interacting serine/threonine protein kinase to activate NFkB. Mitogen activated protein kinases of the MAP3K family are also involved in TNFR1-mediated IKK activation. Mitogen activated kinases can phosphorylate IKK to activate it as well. Activation of Mitogen-activated protein kinase 8 and 14 are involved in the cross-talk of other inflammatory pathways.

PW101496

Pw101496 View Pathway
signaling

TNF/Stress Related Signaling

Mus musculus
Tumour necrosis factor alpha (TNF-a) is a cytokine that activates TNF rector 1 (TNFR1) signalling complex. TNFR1 mediates cell death signalling and inflammation in response to cytokines, bacteria and cellular stress. The classical NFkB pathway involves activation of TNF receptor associated factor 2, receptor interacting serine/threonine protein kinase and death domains which activate the IKK complex, phosphorylating the IKB proteins triggering their degradation resulting in NF-kB dimers dissociation and release. Caspase 2 interacts with TNF-receptor associated factor 2 and receptor interacting serine/threonine protein kinase to activate NFkB. Mitogen activated protein kinases of the MAP3K family are also involved in TNFR1-mediated IKK activation. Mitogen activated kinases can phosphorylate IKK to activate it as well. Activation of Mitogen-activated protein kinase 8 and 14 are involved in the cross-talk of other inflammatory pathways.

PW101511

Pw101511 View Pathway
signaling

TNF/Stress Related Signaling

Bos taurus
Tumour necrosis factor alpha (TNF-a) is a cytokine that activates TNF rector 1 (TNFR1) signalling complex. TNFR1 mediates cell death signalling and inflammation in response to cytokines, bacteria and cellular stress. The classical NFkB pathway involves activation of TNF receptor associated factor 2, receptor interacting serine/threonine protein kinase and death domains which activate the IKK complex, phosphorylating the IKB proteins triggering their degradation resulting in NF-kB dimers dissociation and release. Caspase 2 interacts with TNF-receptor associated factor 2 and receptor interacting serine/threonine protein kinase to activate NFkB. Mitogen activated protein kinases of the MAP3K family are also involved in TNFR1-mediated IKK activation. Mitogen activated kinases can phosphorylate IKK to activate it as well. Activation of Mitogen-activated protein kinase 8 and 14 are involved in the cross-talk of other inflammatory pathways.

PW064784

Pw064784 View Pathway
protein

TNF/Stress Related Signaling

Homo sapiens
Tumour necrosis factor alpha (TNF-a) is a cytokine that activates TNF rector 1 (TNFR1) signalling complex. TNFR1 mediates cell death signalling and inflammation in response to cytokines, bacteria and cellular stress. The classical NFkB pathway involves activation of TNF receptor associated factor 2, receptor interacting serine/threonine protein kinase and death domains which activate the IKK complex, phosphorylating the IKB proteins triggering their degradation resulting in NF-kB dimers dissociation and release. Caspase 2 interacts with TNF-receptor associated factor 2 and receptor interacting serine/threonine protein kinase to activate NFkB. Mitogen activated protein kinases of the MAP3K family are also involved in TNFR1-mediated IKK activation. Mitogen activated kinases can phosphorylate IKK to activate it as well. Activation of Mitogen-activated protein kinase 8 and 14 are involved in the cross-talk of other inflammatory pathways.

PW123662

Pw123662 View Pathway
protein

TNF/Stress Related Signaling 1575850680

Homo sapiens

PW000688

Pw000688 View Pathway
drug action

Tobramycin Action Pathway

Homo sapiens
Tobramycin (also named aktob or tobi) is an aminoglycoside antibiotic that can be used to treat various gram-negative bacterial infections such as the species of Pseudomonas. Bacterial 30S ribosomal subunit protein and four nucleotides of 16S rRNA will be bound with tobramycin irreversibly to cause misreading of mRNA; so that formation of mRNA could be prevented because of incorrect insertion of amino acids to polypeptide will result nonfunctional or toxic peptides. Therefore, there is no protein synthesis for bacteria.

PW128347

Pw128347 View Pathway
drug action

Tobramycin Action Pathway (new)

Homo sapiens
Tobramycin is an antibiotic that is commonly used to treat bacterial infections such as cystic fibrosis-associated bacterial, lower respiratory tract, urinary tract, eye, skin, and bone infections. This drug is a part of the aminoglycoside antibiotics family. It can be administered via inhalation, injection (intravenously or intramuscular), or even via topical cream. Tobramycin acts by binding to bacterial membranes causing displacement of divalent cations and increasing membrane permeability allowing entry into the bacterial cell. Once inside the bacterial cell, tobramycin then targets the bacterial 30S ribosome and binds to it, halting protein synthesis. It binds to the site where the normal base pairing of codon and anti-codon takes place as well as adding amino acids to the growing polypeptide chain, with this blocked it leads to termination of the chain and production of non-functional proteins. The adverse effects of tobramycin are not well known therefore if a patient is experiencing overdose hemodialysis should be performed to clear the excess of tobramycin as they are at risk of nephrotoxicity, ototoxicity, neuromuscular blockade, respiratory paralysis, and/or respiratory failure.

PW144796

Pw144796 View Pathway
drug action

Tobramycin Drug Metabolism Action Pathway

Homo sapiens