Abstract 3972: The role of the TGF-β type III receptor in colon carcinogenesis

2010 ◽  
Author(s):  
Alisha Holtzhausen ◽  
Catherine E. Gatza ◽  
Kellye C. Kirkbride
Keyword(s):  
Colon Carcinogenesis ◽  
Type Iii

The Role of JMJD5 in Colon Carcinogenesis

2015 ◽  
Vol 10 (999) ◽  
pp. 1-1
Author(s):  
Ru Zhang ◽  
Qingjun Huang ◽  
Yinpeng Li ◽  
Yang Song ◽  
Yingxue Li
Keyword(s):  
Colon Carcinogenesis

scholarly journals Role of type III homology repeats in cell adhesive function within the cell-binding domain of fibronectin.

1991 ◽  
Vol 266 (5) ◽  
pp. 3045-3051
Author(s):  
F Kimizuka ◽  
Y Ohdate ◽  
Y Kawase ◽  
T Shimojo ◽  
Y Taguchi ◽  
...  
Keyword(s):  
Binding Domain ◽  
Cell Binding ◽  
Type Iii ◽  
Cell Adhesive ◽  
Cell Binding Domain

scholarly journals Type III Collagen is Required for Adipogenesis and Actin Stress Fibre Formation in 3T3-L1 Preadipocytes

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 156
Author(s):  
Mohammad Al Hasan ◽  
Patricia E. Martin ◽  
Xinhua Shu ◽  
Steven Patterson ◽  
Chris Bartholomew
Keyword(s):  
Quantitative Polymerase Chain Reaction ◽  
Type Iii Collagen ◽  
Type Iii ◽  
Actin Stress Fibre ◽  
Matrix Gene ◽  
Gene Transcripts ◽  
Polymerase Chain ◽  
Oil Red O Staining ◽  
Oil Red O

GPR56 is required for the adipogenesis of preadipocytes, and the role of one of its ligands, type III collagen (ColIII), was investigated here. ColIII expression was examined by reverse transcription quantitative polymerase chain reaction, immunoblotting and immunostaining, and its function investigated by knockdown and genome editing in 3T3-L1 cells. Adipogenesis was assessed by oil red O staining of neutral cell lipids and production of established marker and regulator proteins. siRNA-mediated knockdown significantly reduced Col3a1 transcripts, ColIII protein and lipid accumulation in 3T3-L1 differentiating cells. Col3a1−/− 3T3-L1 genome-edited cell lines abolished adipogenesis, demonstrated by a dramatic reduction in adipogenic moderators: Pparγ2 (88%) and C/ebpα (96%) as well as markers aP2 (93%) and oil red O staining (80%). Col3a1−/− 3T3-L1 cells displayed reduced cell adhesion, sustained active β-catenin and deregulation of fibronectin (Fn) and collagen (Col4a1, Col6a1) extracellular matrix gene transcripts. Col3a1−/− 3T3-L1 cells also had dramatically reduced actin stress fibres. We conclude that ColIII is required for 3T3-L1 preadipocyte adipogenesis as well as the formation of actin stress fibres. The phenotype of Col3a1−/− 3T3-L1 cells is very similar to that of Gpr56−/− 3T3-L1 cells, suggesting a functional relationship between ColIII and Gpr56 in preadipocytes.

scholarly journals Two Enteropathogenic Escherichia coli Type III Secreted Proteins, EspA and EspB, Are Virulence Factors

1998 ◽  
Vol 188 (10) ◽  
pp. 1907-1916 ◽  
Author(s):  
Akio Abe ◽  
Ursula Heczko ◽  
Richard G. Hegele ◽  
B. Brett Finlay
Keyword(s):  
Escherichia Coli ◽  
Virulence Factors ◽  
Enterohemorrhagic Escherichia Coli ◽  
Laser Scanning Microscopy ◽  
Secreted Proteins ◽  
Confocal Laser ◽  
Infection Model ◽  
Enteropathogenic Escherichia Coli ◽  
Type Iii

Enteropathogenic Escherichia coli (EPEC) belongs to a family of related bacterial pathogens, including enterohemorrhagic Escherichia coli (EHEC) O157:H7 and other human and animal diarrheagenic pathogens that form attaching and effacing (A/E) lesions on host epithelial surfaces. Bacterial secreted Esp proteins and a type III secretion system are conserved among these pathogens and trigger host cell signal transduction pathways and cytoskeletal rearrangements, and mediate intimate bacterial adherence to epithelial cell surfaces in vitro. However, their role in pathogenesis is still unclear. To investigate the role of Esp proteins in disease, mutations in espA and espB were constructed in rabbit EPEC serotype O103 and infection characteristics were compared to that of the wild-type strain using histology, scanning and transmission electron microscopy, and confocal laser scanning microscopy in a weaned rabbit infection model. The virulence of EspA and EspB mutant strains was severely attenuated. Additionally, neither mutant strain formed A/E lesions, nor did either one cause cytoskeletal actin rearrangements beneath the attached bacteria in the rabbit intestine. Collectively, this study shows for the first time that the type III secreted proteins EspA and EspB are needed to form A/E lesions in vivo and are indeed virulence factors. It also confirms the role of A/E lesions in disease processes.

scholarly journals Induction of Dendritic Cell Production of Type I and Type III Interferons by Wild-Type and Vaccine Strains of Measles Virus: Role of Defective Interfering RNAs

2013 ◽  
Vol 87 (14) ◽  
pp. 7816-7827 ◽  
Author(s):  
R. Shivakoti ◽  
M. Siwek ◽  
D. Hauer ◽  
K. L. W. Schultz ◽  
D. E. Griffin
Keyword(s):  
Dendritic Cell ◽  
Measles Virus ◽  
Type I ◽  
Wild Type ◽  
Cell Production ◽  
Type Iii

scholarly journals NO-Donating NSAIDs, PPARδ, and Cancer: Does PPARδContribute to Colon Carcinogenesis?

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-11 ◽  
Author(s):  
Gerardo G. Mackenzie ◽  
Shaheen Rasheed ◽  
William Wertheim ◽  
Basil Rigas
Keyword(s):  
Cancer Biology ◽  
Antitumor Effect ◽  
Colon Carcinogenesis ◽  
Wild Type ◽  
Antineoplastic Effect ◽  
Intestinal Neoplasia ◽  
Chemopreventive Effect ◽  
The Relationship ◽  
Epithelial Cell Death

The chemopreventive NO-donating NSAIDs (NO-NSAIDs; NSAIDs with an NO-releasing moiety) modulate PPARδand offer the opportunity to revisit the controversial role of PPARδin carcinogenesis (several papers report that PPARδeither promotes or inhibits cancer). This review summarizes the pharmacology of NO-NSAIDs, PPARδcancer biology, and the relationship between the two. In particular, a study of the chemopreventive effect of two isomers of NO-aspirin on intestinal neoplasia inMinmice showed that, compared to wild-type controls, PPARδis overexpressed in the intestinal mucosa ofMinmice; PPARδresponds tom- andp-NO-ASA proportionally to their antitumor effect (p->m-). This effect is accompanied by the induction of epithelial cell death, which correlates with the antineoplastic effect of NO-aspirin; and NO-aspirin's effect on PPARδis specific (no changes in PPARαor PPARγ). Although these data support the notion that PPARδpromotes intestinal carcinogenesis and its inhibition could be therapeutically useful, more work is needed before a firm conclusion is reached.

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