scholarly journals Corrigendum to “Wingless-Type MMTV Integration Site Family Member 5a Is a Key Secreted Islet Stellate Cell-Derived Product that Regulates Islet Function”

2019 ◽  
Vol 2019 ◽  
pp. 1-3
Author(s):  
Wei Xu ◽  
Jun Liang ◽  
H. F. Geng ◽  
Jun Lu ◽  
Rui Li ◽  
...  
Keyword(s):  
Family Member ◽  
Stellate Cell ◽  
Integration Site ◽  
Islet Function

scholarly journals Wingless-Type MMTV Integration Site Family Member 5a Is a Key Secreted Islet Stellate Cell-Derived Product that Regulates Islet Function

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Wei Xu ◽  
Jun Liang ◽  
H. F. Geng ◽  
Jun Lu ◽  
Rui Li ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Family Member ◽  
Stellate Cell ◽  
Integration Site ◽  
Islet Function ◽  
Insulin Production ◽  
The Status ◽  
Secretory Products

Background. Emerging evidence suggests that T2DM is attributable to the dysfunction of β-cells and the activation of islet stellate cells (ISCs). The wingless-type MMTV integration site family member 5a (Wnt5a)/frizzled 5 (Fzd5) signalling pathway might take part in this process. Our study is aimed at defining the status of ISCs during β-cell insulin secretion homeostasis by determining the role of the Wnt5a protein in the regulation of insulin production. We examined the effects of the status of ISCs on β-cell insulin secretion in normoglycemic db/m and hyperglycaemic db/db mice. Methods. iTRAQ protein screening and RNA interference were used to determine novel ISC-derived secretory products that may use other mechanisms to influence the function of islets. Results. We showed a significant reduction in insulin secretion by β-cells in vitro when they were cocultured with db/db ISCs compared to when they were cocultured with ISCs isolated from normoglycemic db/m mice; in addition, both Wnt5a and its receptor Fzd5 were more highly expressed by quiescent ISCs than by activated db/db ISCs. Treatment with exogenous Wnt5a increased the secretion of insulin in association with the deactivation of ISCs. Conclusion. Our observations revealed that the Wnt5a protein is a key effector of ISC-mediated improvement in islet function.

Congenital Duplication of the Palm in a Patient with Multiple Anomalies

2003 ◽  
Vol 28 (3) ◽  
pp. 276-279 ◽  
Author(s):  
M. M. AL-QATTAN
Keyword(s):  
Family Member ◽  
Integration Site ◽  
Mammary Tumour ◽  
Mouse Mammary Tumour Virus ◽  
Virus Integration ◽  
Virus Integration Site

In 1995, Parr and McMahon described a syndrome of congenital duplication of footpads in mice which lacked a protein called ‘Wingless-type mouse mammary tumour virus integration site family member 7a” (Wnt-7a). This syndrome has not been described in humans and the following report describes a similar syndrome in a Saudi girl. The role of Wnt-7a in the development of the limb along the dorso-ventral axis is discussed, along with interaction between the Wnt-7a and other axes of limb growth.

scholarly journals Pelacakan Protein Wingless-Type MMTV Integration Site Family Member-4 pada Uterus Mencit (DETECTION WINGLESS-TYPE MMTV INTEGRATION SITE FAMILY MEMBER-4 PROTEIN OF MOUSE UTERUS)

2016 ◽  
Vol 17 (1) ◽  
pp. 71-77
Author(s):  
Agung Janika Sitasiwi ◽  
◽  
Wayan Tunas Artama ◽  
Agung Budiyanto ◽  
Edy Dharmana ◽  
...  
Keyword(s):  
Family Member ◽  
Integration Site ◽  
Mouse Uterus

scholarly journals Wingless‐type MMTV integration site family member 5a is a key inhibitor of islet stellate cells activation

2019 ◽  
Vol 11 (2) ◽  
pp. 307-314 ◽  
Author(s):  
Wei Xu ◽  
HouFa Geng ◽  
Jun Liang ◽  
Ying Liu ◽  
Qian Lv ◽  
...  
Keyword(s):  
Family Member ◽  
Integration Site ◽  
Stellate Cells

scholarly journals Association of the Gene Encoding Wingless-Type Mammary Tumor Virus Integration-Site Family Member 5B (WNT5B) with Type 2 Diabetes

2004 ◽  
Vol 75 (5) ◽  
pp. 832-843 ◽  
Author(s):  
Akio Kanazawa ◽  
Syuuichi Tsukada ◽  
Akihiro Sekine ◽  
Tatsuhiko Tsunoda ◽  
Atsushi Takahashi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Family Member ◽  
Mammary Tumor ◽  
Integration Site ◽  
Gene Encoding ◽  
Mammary Tumor Virus ◽  
Tumor Virus ◽  
Virus Integration ◽  
Virus Integration Site
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