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
= "Q99706"
uniprot_id = fetch_uniprot_data(uniprot_id)
data display_uniprot_data(data)
UniProt ID: Q99706
Protein Name: Killer cell immunoglobulin-like receptor 2DL4
Organism: Homo sapiens
Function: Receptor for non-classical major histocompatibility class Ib HLA-G molecules. Recognizes HLA-G in complex with B2M/beta-2 microglobulin and a nonamer self-peptide (peptide-bound HLA-G-B2M). In decidual NK cells, binds peptide-bound HLA-G-B2M complex and triggers NK cell senescence-associated secretory phenotype as a molecular switch to promote vascular remodeling and fetal growth in early pregnancy (PubMed:16366734, PubMed:23184984, PubMed:29262349). May play a role in balancing tolerance and antiviral-immunity at maternal-fetal interface by keeping in check the effector functions of NK, CD8+ T cells and B cells (PubMed:10190900, PubMed:16366734). Upon interaction with peptide-bound HLA-G-B2M, initiates signaling from the endosomal compartment leading to downstream activation of PRKDC-XRCC5 and AKT1, and ultimately triggering NF-kappa-B-dependent pro-inflammatory response (PubMed:20179272)