EX NO.

: 11 KEGG
DATE:

AIM: To learn about protein pathway analysis using KEGG database

THEORY: KEGG stands for Kyoto Encyclopedia of Genes and Genomes. KEGG is a database
resource for understanding high-level functions and utilities of the biological system, such as the cell,
the organism and the ecosystem, from molecular-level information, especially large-scale molecular
datasets generated by genome sequencing and other high-throughput experimental technologies.

PROCEDURE:
1. Download the FASTA sequences of a diseases related protein (Alzheimer's) from a single
organism in the form of a list file from uniprot.
2. Open KEGG database and click on ti the tools from the toolbar; go to convert ID and
paste the uniprot ID of the organism in the box displayed.
3. Change the settings to uniprot, select gene and execute.
4. ID conversion result will appear; “KO“ value; which must be notted down.
5. Click on the tools, select mapper and then reconstruct. Paste the gene name and KO value
and click execute.
6. A chart will appear with disease name. By clicking on to the disease we can get its
pathway, type of gene responsible and its role.

OBSERVATION:
Name: Alzheimer disease Organism: Homo sapiens (human)
1. GENETIC INFORMATION PROCESSING:
Chromosome:
03082 ATP - dependant chromatin remodelling
2. ENVIRONMENTAL INFORMATION PROCESSING:
04330 Notch signaling:
K04505 PSEN1
K04522 PSEN2
3. CELLULAR METABOLISM:
Transport and catabolism:
04145 Phagosome
K10062 COLEC12
4. ORGANISMAL SYSTEMS:
04380 osteoclast differentiation:
K07992 TYROBP
K14378 TREM2
5. HUMAN DISEASES:
Neurodegenerative diseases:
05010 Alzhemir’s disease
K04505 PSEN1
K04520 APP
K04522 PSEN2
Description:
Alzheimer disease (AD) is a chronic disorder that slowly destroys neurons and causes serious cognitive
disability. AD is associated with senile plaques and neurofibrillary tangles (NFTs). Amyloid-beta (Abeta), a
major component of senile plaques, has various pathological effects on cell and organelle function. To date
genetic studies have revealed four genes that may be linked to autosomal dominant or familial early onset AD
(FAD). These four genes include: amyloid precursor protein (APP), presenilin 1 (PS1), presenilin 2 (PS2) and
apolipoprotein E (ApoE). All mutations associated with APP and PS proteins can lead to an increase in the
production of Abeta peptides, specfically the more amyloidogenic form, Abeta42. It was proposed that Abeta
form Ca2+ permeable pores and bind to and modulate multiple synaptic proteins, including NMDAR,
mGluR5 and VGCC, leading to the overfilling of neurons with calcium ions. Consequently, cellular Ca2+
disruptions will lead to neuronal apoptosis, autophagy deficits, mitochondrial abnormality, defective
neurotransmission, impaired synaptic plasticity and neurodegeneration in AD. FAD-linked PS1 mutation
downregulates the unfolded protein response and leads to vulnerability to ER stress.

Pathway map:
INTERPRETATION:
For the selective prefix of human organism the keyword used was “hum” according to which the organism
related pathways will be visualized. With the assistance of the “organism” icon the keyword has been obtained
and the pathways of Alzheimer disease has been entered and the respective criteria asked were entered with the
structure of pathways and the gene sequences.

RESULTS: The Alzheimer disease in the organism Homo sapiens has been interpreted successfully with the
data for the pathway identifier.