scholarly article | Q13442814 |
P50 | author | Keisuke Horiuchi | Q42877478 |
Tetsuya Tsukamoto | Q43285168 | ||
Yasunori Okada | Q50629396 | ||
P2093 | author name string | Masayuki Shimoda | |
Yuko Kitagawa | |||
Hirotoshi Hasegawa | |||
Koji Okabayashi | |||
Aya Sasaki | |||
P2860 | cites work | Tumour necrosis factor alpha converting enzyme (TACE) activity in the colonic mucosa of patients with inflammatory bowel disease | Q24669999 |
Review article: the role of anti-TNF in the management of ulcerative colitis -- past, present and future | Q26992012 | ||
A metalloproteinase disintegrin that releases tumour-necrosis factor-alpha from cells | Q28119154 | ||
The ADAM metalloproteinases | Q28292696 | ||
ADAMs: key components in EGFR signalling and development | Q28305519 | ||
Binding of ADAM28 to P-selectin glycoprotein ligand-1 enhances P-selectin-mediated leukocyte adhesion to endothelial cells | Q28307734 | ||
Inducible gene targeting in mice | Q29614544 | ||
Inflammatory bowel disease | Q29616286 | ||
Distinct roles for ADAM10 and ADAM17 in ectodomain shedding of six EGFR ligands | Q30443463 | ||
Epidermal ADAM17 maintains the skin barrier by regulating EGFR ligand-dependent terminal keratinocyte differentiation | Q30515730 | ||
Systemic responses of mice to dextran sulfate sodium-induced acute ulcerative colitis using 1H NMR spectroscopy | Q30621911 | ||
TACE (ADAM17) inhibits Schwann cell myelination | Q33930447 | ||
iRHOM2-dependent regulation of ADAM17 in cutaneous disease and epidermal barrier function | Q33947954 | ||
Critical role of the disintegrin metalloprotease ADAM17 for intestinal inflammation and regeneration in mice | Q34044458 | ||
TACE/ADAM17 is essential for oligodendrocyte development and CNS myelination | Q34123782 | ||
MyD88 signaling in nonhematopoietic cells protects mice against induced colitis by regulating specific EGF receptor ligands | Q34358637 | ||
The ADAMs family of proteases: new biomarkers and therapeutic targets for cancer? | Q35206311 | ||
Differential expression of multiple transglutaminases in human colon: impaired keratinocyte transglutaminase expression in ulcerative colitis | Q35597293 | ||
Skin manifestations of inflammatory bowel disease | Q35740427 | ||
Loss of ADAM17-Mediated Tumor Necrosis Factor Alpha Signaling in Intestinal Cells Attenuates Mucosal Atrophy in a Mouse Model of Parenteral Nutrition | Q36109388 | ||
Differentiation-induced skin cancer suppression by FOS, p53, and TACE/ADAM17. | Q36129113 | ||
Cellular and molecular mechanisms of the epithelial repair in IBD. | Q36268040 | ||
ADAMs in cancer cell proliferation and progression. | Q36758613 | ||
Role of the intestinal barrier in inflammatory bowel disease | Q37058869 | ||
ADAM17 controls endochondral ossification by regulating terminal differentiation of chondrocytes | Q37122908 | ||
The ADAMs: signalling scissors in the tumour microenvironment | Q37324256 | ||
Importance of mucosal healing in ulcerative colitis | Q37564311 | ||
Dextran sulfate sodium (DSS)-induced colitis in mice | Q37693428 | ||
ADAM17: a molecular switch to control inflammation and tissue regeneration | Q37900757 | ||
Proteolytic factors in exosomes | Q38092801 | ||
Metalloproteinases and their natural inhibitors in inflammation and immunity. | Q38130854 | ||
Intestinal epithelial cells: regulators of barrier function and immune homeostasis | Q38190874 | ||
Epidemiology and risk factors for IBD. | Q38366954 | ||
Loss of the Timp gene family is sufficient for the acquisition of the CAF-like cell state | Q38963422 | ||
Differential expression and regulation of ADAM17 and TIMP3 in acute inflamed intestinal epithelia | Q39870713 | ||
Reduced susceptibility of mice overexpressing transforming growth factor alpha to dextran sodium sulphate induced colitis | Q41820837 | ||
Chemically induced mouse models of intestinal inflammation | Q42510602 | ||
Inflammatory skin and bowel disease linked to ADAM17 deletion | Q43484128 | ||
Conditional gene targeting in macrophages and granulocytes using LysMcre mice. | Q44554898 | ||
Clinical patterns, natural history, and progression of ulcerative colitis | Q61698960 | ||
The human intestinal cell lines Caco-2 and LS174T as models to study cell-type specific mucin expression | Q71762344 | ||
Mice lacking transforming growth factor alpha have an increased susceptibility to dextran sulfate-induced colitis | Q73675999 | ||
An essential role for ectodomain shedding in mammalian development | Q77544828 | ||
Ectodomain shedding of the EGF-receptor ligand epigen is mediated by ADAM17 | Q79433646 | ||
Cutting edge: TNF-alpha-converting enzyme (TACE/ADAM17) inactivation in mouse myeloid cells prevents lethality from endotoxin shock | Q80819547 | ||
Hypoxia-inducible factor mediates hypoxic and tumor necrosis factor alpha-induced increases in tumor necrosis factor-alpha converting enzyme/ADAM17 expression by synovial cells | Q81331569 | ||
Ulcerative colitis | Q84851901 | ||
P921 | main subject | inflammation | Q101991 |
P304 | page(s) | 114-124 | |
P577 | publication date | 2016-02-09 | |
P1433 | published in | EBioMedicine | Q24912341 |
P1476 | title | Epithelial Cell-Derived a Disintegrin and Metalloproteinase-17 Confers Resistance to Colonic Inflammation Through EGFR Activation | |
P478 | volume | 5 |
Q49307913 | ADAM17 is a Tumor Promoter and Therapeutic Target in Western Diet-associated Colon Cancer |
Q61809339 | CD9 regulates keratinocyte migration by negatively modulating the sheddase activity of ADAM17 |
Q92024709 | Covid-19 and immunomodulation in IBD |
Q33755171 | Growth Hormone Resistance-Special Focus on Inflammatory Bowel Disease. |
Q57064857 | Human rhomboid family-1 modulates clathrin coated vesicle-dependent pro-transforming growth factor α membrane trafficking to promote breast cancer progression |
Q47220619 | Loss of PACS-2 delays regeneration in DSS-induced colitis but does not affect the ApcMin model of colorectal cancer |
Q90320514 | Reciprocal control of ADAM17/EGFR/Akt signaling and miR-145 drives GBM invasiveness |
Q42233374 | Zeolite-Containing Mixture Supplementation Ameliorated Dextran Sodium Sulfate-Induced Colitis in Mice by Suppressing the Inflammatory Bowel Disease Pathway and Improving Apoptosis in Colon Mucosa |
Search more.