This volume focuses on the investigatory methods applied to autosomal dominant polycystic kidney disease (ADPKD), one of the most common human genetic diseases. ADPKD is caused by mutations in PKD1 and TRPP2, two integral membrane proteins that function as receptor/ion channels in primary cilia of tubular epithelial cells. Thus, ADPKD belongs to ciliopathies, a group of disorders caused by abnormal cilia formation or function. This proposed book will cover the state-of-the-art methods ranging from molecular biology, biochemistry, electrophysiology, to tools in model animal studies.
Key Features
Explores the role of cilia in polycystic kidney disease
Focuses on myriad state-of-the-art methods and techniques
Reviews specific mutations integral to this autosomal genetic disease
Includes discussions of model systems
- ISBN:
- 9781138603899
- 9781138603899
-
Category:
- Renal medicine & nephrology
- Format:
- Hardback
- Publication Date:
-
30-11-2019
- Publisher:
- Taylor & Francis Ltd
- Country of origin:
- United Kingdom
- Pages:
- 360
- Dimensions (mm):
- 234x156mm
- Weight:
- 0.75kg
This title is in stock with our Australian supplier and should arrive at our Sydney warehouse within 2 - 3 weeks of you placing an order.
Once received into our warehouse we will despatch it to you with a Shipping Notification which includes online tracking.
Please check the estimated delivery times below for your region, for after your order is despatched from our warehouse:
ACT Metro: 2 working days
NSW Metro: 2 working days
NSW Rural: 2-3 working days
NSW Remote: 2-5 working days
NT Metro: 3-6 working days
NT Remote: 4-10 working days
QLD Metro: 2-4 working days
QLD Rural: 2-5 working days
QLD Remote: 2-7 working days
SA Metro: 2-5 working days
SA Rural: 3-6 working days
SA Remote: 3-7 working days
TAS Metro: 3-6 working days
TAS Rural: 3-6 working days
VIC Metro: 2-3 working days
VIC Rural: 2-4 working days
VIC Remote: 2-5 working days
WA Metro: 3-6 working days
WA Rural: 4-8 working days
WA Remote: 4-12 working days
Share This Book: