Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.2.1.36 (
hyaluronidase
)
4,606
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Esterase release was investigated in male and female submandibular glands of 5 strains of mice (ICR/BR, ND/4BR, SW/BR,
DDS
/Cox and C57BL/6BR) using dispersed cells prepared by treatment with collagenase and
hyaluronidase
. The muscarinic-cholinergic agonist methacholine stimulated esterase release in C57BL/6BR,
DDS
/Cox and SW/BR females and
DDS
/Cox males in a dose-dependent manner, but did not stimulate esterase release in ICR/BR and ND/4BR strains of both sexes. The percentage release of esterase over control in response to methacholine in females was of the descending order: C57BL/6BR,
DDS
/Cox, SW/BR, ND/4BR, ICR/BR. There was a close relationship between the percentage release of esterase by methacholine and the esterase activity in homogenate of submandibular gland. The lower the esterase content in the homogenate of mouse submandibular gland, the higher the percentage release of esterase by methacholine stimulation in the dispersed cells.
...
PMID:Intraspecies variation in methacholine-stimulated esterase release from mouse submandibular gland. 634 93
Hyaluronic acid (HA), a constituent of the extracellular matrix, promotes colorectal cancer growth. CD44 is a relevant HA receptor in this context. However, HA is also a ligand for TLR4, a receptor of significance in colorectal cancer. In this study, we examine the relative contribution of HA interactions with CD44 and TLR4 in colon tumorigenesis. Colorectal cancer models included Apc
Min/+
mice, azoxymethane/dextran sodium sulfate (AOM-DSS), and CT26 tumor isografts. We used knockout mice and CT26 colorectal cancer cells with CRISPR knockdown of CD44 and TLR4. HA activity was modulated by PEP1 (a 12-mer peptide that blocks HA from binding its receptors),
hyaluronidase
(which promotes HA degradation), or 4-MU (HA synthesis inhibitor). Blockade of HA binding via PEP1 decreased growth in all colorectal cancer models and in cell culture. The effects were significant in WT and with CD44 deletion, but not with TLR4 deletion. In the AOM-
DSS
model, mice deficient in CD44 or TLR4 had fewer tumors. CD44- and TLR4-deficient CT26 isografts grew more slowly, exhibiting decreased tumor cell proliferation and increased apoptosis.
In vitro
, endogenous HA blocked LPS binding to TLR4 suggesting that HA is a relevant TLR4 ligand in colon cancer. Finally, PEP1 enhanced tumor radiation sensitivity in the isograft model. Together, these results indicate that HA binding to TLR4, as well as CD44, plays a key role in colon tumorigenesis. These findings also raise the possibility that an agent that blocks HA binding, such as PEP1, may be useful as an adjuvant therapy in colon cancer.
...
PMID:Hyaluronic Acid Binding to TLR4 Promotes Proliferation and Blocks Apoptosis in Colon Cancer. 3148 4
