A collagen peptide motif activates calcium signalling in SaOS-2 cells

1995 ◽  
Vol 23 (3) ◽  
pp. 404S-404S ◽  
Author(s):  
TERRY McCANN ◽  
MURRAY C MEIKLE ◽  
ANDREW J NORTHROP ◽  
WILLIAM T MASON ◽  
FRASER McDONALD
Keyword(s):  
Calcium Signalling ◽  
Peptide Motif ◽  
Collagen Peptide

Inositol lipids and TRPC channel activation

2007 ◽  
Vol 74 ◽  
pp. 37-45 ◽  
Author(s):  
James W. Putney
Keyword(s):  
Plasma Membrane ◽  
Phospholipase C ◽  
Transient Receptor Potential ◽  
Calcium Signalling ◽  
Receptor Potential ◽  
Breakdown Product ◽  
Channel Activation ◽  
Inositol Lipids ◽  
Transient Receptor ◽  
Secondary Mechanism

The original hypothesis put forth by Bob Michell in his seminal 1975 review held that inositol lipid breakdown was involved in the activation of plasma membrane calcium channels or ‘gates’. Subsequently, it was demonstrated that while the interposition of inositol lipid breakdown upstream of calcium signalling was correct, it was predominantly the release of Ca2+ that was activated, through the formation of Ins(1,4,5)P3. Ca2+ entry across the plasma membrane involved a secondary mechanism signalled in an unknown manner by depletion of intracellular Ca2+ stores. In recent years, however, additional non-store-operated mechanisms for Ca2+ entry have emerged. In many instances, these pathways involve homologues of the Drosophila trp (transient receptor potential) gene. In mammalian systems there are seven members of the TRP superfamily, designated TRPC1–TRPC7, which appear to be reasonably close structural and functional homologues of Drosophila TRP. Although these channels can sometimes function as store-operated channels, in the majority of instances they function as channels more directly linked to phospholipase C activity. Three members of this family, TRPC3, 6 and 7, are activated by the phosphoinositide breakdown product, diacylglycerol. Two others, TRPC4 and 5, are also activated as a consequence of phospholipase C activity, although the precise substrate or product molecules involved are still unclear. Thus the TRPCs represent a family of ion channels that are directly activated by inositol lipid breakdown, confirming Bob Michell's original prediction 30 years ago.

Upregulation of MUC3 mucin expression from a unique peptide motif of mammary-associated amyloid (MAA) from bovine colostrum

2001 ◽  
Vol 120 (5) ◽  
pp. A673-A674
Author(s):  
D MACK ◽  
M LARSON ◽  
S WEI ◽  
A WEBER ◽  
T MCDONALD
Keyword(s):  
Bovine Colostrum ◽  
Peptide Motif ◽  
Unique Peptide ◽  
Mucin Expression

New Insights on KCa3.1 Channel Modulation

2020 ◽  
Vol 26 (18) ◽  
pp. 2096-2101
Author(s):  
Giuseppe Manfroni ◽  
Francesco Ragonese ◽  
Lorenzo Monarca ◽  
Andrea Astolfi ◽  
Loretta Mancinelli ◽  
...  
Keyword(s):  
Potassium Channel ◽  
Critical Role ◽  
Calcium Signalling ◽  
Typical Feature ◽  
Open Probability ◽  
Pharmacological Agents ◽  
Channel Modulation ◽  
Calcium Dependent ◽  
Modelling Techniques ◽  
Calcium Activated Potassium Channel

The human intermediate conductance calcium-activated potassium channel, KCa3.1, is involved in several pathophysiological conditions playing a critical role in cell secretory machinery and calcium signalling. The recent cryo-EM analysis provides new insights for understanding the modulation by both endogenous and pharmacological agents. A typical feature of this channel is the low open probability in saturating calcium concentrations and its modulation by potassium channel openers (KCOs), such as benzo imidazolone 1-EBIO, without changing calcium-dependent activation. In this paper, we proposed a model of KCOs action in the modulation of channel activity. The KCa3.1 channel has a very rich pharmacological profile with several classes of molecules that selectively interact with different binding sites of the channel. Among them, benzo imidazolones can be openers (positive modulators such as 1-EBIO, DC-EBIO) or blockers (negative modulators such as NS1619). Through computation modelling techniques, we identified the 1,4-benzothiazin-3-one as a promising scaffold to develop new KCa3.1 channel modulators. Further studies are needed to explore the potential use of 1-4 benzothiazine- 3-one in KCa3.1 modulation and its pharmacological application.

scholarly journals Light-controlled calcium signalling in prostate cancer and benign prostatic hyperplasia

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Vipin Sharma ◽  
Rita Rana ◽  
Ruma Baksi ◽  
Swapnil P. Borse ◽  
Manish Nivsarkar
Keyword(s):  
Prostate Cancer ◽  
Benign Prostatic Hyperplasia ◽  
Calcium Signalling ◽  
Prostatic Hyperplasia

TYPE III PRO-COLLAGEN PEPTIDE IN LIVER DISEASE IN HAEMOPHILIA

1987 ◽  
Author(s):  
R S Evely ◽  
F E Preston ◽  
D R Triger ◽  
C R M Hay ◽  
M C Greves ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Biopsy ◽  
Statistical Significance ◽  
Type Iii ◽  
Amino Terminal ◽  
Collagen Peptide ◽  
Collagen Iii ◽  
Liver Biopsies ◽  
Progressive Liver Disease ◽  
Valuable Predictor

During the past 10 years we have carried out liver biopsies on haemophiliacs with biochemical evidence of chronic liver disease (CLD). To date 44 biopsies have been obtained from 35 patients. Histological diagnoses are Chronic Persistent Hepatitis (CPH) 24, Chronic Aggressive Hepatitis (CAH) 11 and Cirrhosis 9. Serial biopsies indicate that progressive liver disease is now a serious problem in haemophilia. Liver biopsy is not without risk and therefore it is important to identify factors which may be of value in predicting the nature of the liver disease or its progression. Since intra-hepatic fibrosis is a feature of CLD we measured Type III amino terminal propeptide of pro-collagen (PC III) by radio-immunoassay on samples taken within a mean of 4.8 months of the liver biopsy. A normal range was established as 4.3 - 15.7ng/ml on healthy subjects (median 7.0). Median values and ranges for patients with CPH (N=13), CAH (N=5) and cirrhosis (N=5) were 8 (5.4 - 23.4), 14.2 (7.2 - 19.8) and 14.2 (11.2 - 23.0)ng/ml respectively. Although pro-collagen III values tended to be higher in progressive liver disease (CAH and cirrhosis) this did not reach statistical significance. It would, therefore, appear that unlike serum IgG, pro-collagen III will not be a valuable predictor of progressive liver disease in haemophilia. A larger study is necessary to clarify this.

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