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Chymotrypsinogen B1

From Wikipedia, the free encyclopedia
(Redirected from CTRB1)
CTRB1
Identifiers
AliasesCTRB1, CTRB, chymotrypsinogen B1
External IDsOMIM: 118890; MGI: 88559; GeneCards: CTRB1
Enzyme activity
EC #BRENDAExPASyKEGGMetaCyc
3.4.21.1↗↗↗↗
Orthologs
DatabasesNCBI: entry; OMA: entry
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001906
NM_001329190

NM_025583

RefSeq (protein)

NP_001316119
NP_001897

NP_079859

Location (UCSC)Chr 16: 75.22 – 75.23 MbChr 8: 112.41 – 112.42 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Chymotrypsinogen B1 (or sometimes just Chymotrypsinogen B) is a protein that in humans is encoded by the CTRB1 gene.[5] Similar to its paralog chymotrypsinogen B2, chymotrypsiongen B1 is an inactive precursor for an enzyme which is an isozyme of chymotrypsin.[6] It is secreted by the acinar cells of the pancreas into the small intestines as part of pancreatic juice, where it is activated.[5][7] After activation it functions as a protease which is involved in breaking down other proteins as part of digestion.[5]

Medical significance

[edit]

The CTRB1 and CTRB2 genes are located near each other on chromosome 16.[5] In some populations there is an inversion which causes certain parts of each gene to be swapped, which has been associated with an increased risk of chronic pancreatitis.[5]

References

[edit]
  1. 1 2 3 ENSG00000285346 GRCh38: Ensembl release 89: ENSG00000168925, ENSG00000285346 – Ensembl, May 2017
  2. 1 2 3 GRCm38: Ensembl release 89: ENSMUSG00000031957 – Ensembl, May 2017
  3. ↑ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ↑ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. 1 2 3 4 5 "Entrez Gene: Chymotrypsinogen B1". Retrieved 2026-09-01.
  6. ↑ "P17538 · CTRB1_HUMAN". uniprot.org. UniProt consortium. Retrieved 2026-09-01.
  7. ↑ Pandol SJ (2010). "Anatomy". The Exocrine Pancreas. Morgan & Claypool Life Science.