Code
import requests
import urllib3
urllib3.disable_warnings()
def fetch_uniprot_data(uniprot_id):
= f"https://rest.uniprot.org/uniprotkb/{uniprot_id}.json"
url = requests.get(url, verify=False) # Disable SSL verification
response # Raise an error for bad status codes
response.raise_for_status() return response.json()
def display_uniprot_data(data):
= data.get('primaryAccession', 'N/A')
primary_accession = data.get('proteinDescription', {}).get('recommendedName', {}).get('fullName', {}).get('value', 'N/A')
protein_name = data.get('gene', [{'geneName': {'value': 'N/A'}}])[0]['geneName']['value']
gene_name = data.get('organism', {}).get('scientificName', 'N/A')
organism
= next((comment for comment in data.get('comments', []) if comment['commentType'] == "FUNCTION"), None)
function_comment = function_comment['texts'][0]['value'] if function_comment else 'N/A'
function
# Printing the data
print(f"UniProt ID: {primary_accession}")
print(f"Protein Name: {protein_name}")
print(f"Organism: {organism}")
print(f"Function: {function}")
# Replace this with the UniProt ID you want to fetch
= "P15260"
uniprot_id = fetch_uniprot_data(uniprot_id)
data display_uniprot_data(data)
UniProt ID: P15260
Protein Name: Interferon gamma receptor 1
Organism: Homo sapiens
Function: Receptor subunit for interferon gamma/INFG that plays crucial roles in antimicrobial, antiviral, and antitumor responses by activating effector immune cells and enhancing antigen presentation (PubMed:20015550). Associates with transmembrane accessory factor IFNGR2 to form a functional receptor (PubMed:10986460, PubMed:2971451, PubMed:7615558, PubMed:7617032, PubMed:7673114). Upon ligand binding, the intracellular domain of IFNGR1 opens out to allow association of downstream signaling components JAK1 and JAK2. In turn, activated JAK1 phosphorylates IFNGR1 to form a docking site for STAT1. Subsequent phosphorylation of STAT1 leads to dimerization, translocation to the nucleus, and stimulation of target gene transcription (PubMed:28883123). STAT3 can also be activated in a similar manner although activation seems weaker. IFNGR1 intracellular domain phosphorylation also provides a docking site for SOCS1 that regulates the JAK-STAT pathway by competing with STAT1 binding to IFNGR1 (By similarity)