Synonym |
Salusin-beta |
Species |
Human |
Protein Accession |
P0DPB0 |
Purity |
Greater than 95% as determined by SDS-PAGE |
Endotoxin Level |
Less than 1 EU/μg |
Biological Activity |
Not available |
Expression System |
E. coli |
Fusion Tag |
None |
Predicted Molecular Mass |
2.3 kDa |
Formulation |
Lyophilized from a 0.2 μm filtered solution in Acetonitrile and TFA |
Reconstitution |
Centrifuge vial before opening. Reconstitute in sterile distilled water to a concentration of
0.1-1.0 mg/ml. |
Storage & Stability |
Store at -80°C. Avoid repeated freeze-thaw cycles. |
FAQ
What exactly is Salusin-β (human), and how does it differ from other similar compounds?
Salusin-β
(human) is a bioactive peptide that plays an intriguing role in human physiology and is distinct from
its counterpart, Salusin-α. Salusin-β, like Salusin-α, is derived from a prosalusin precursor peptide
via specific enzymatic processes. However, Salusin-β is particularly fascinating due to its unique
structural properties and biological activities which set it apart from Salusin-α. Salusin-β comprises a
different sequence of amino acids that confer upon it diverse physiological effects, including
authoritative roles in cardiovascular and metabolic regulation.
A significant distinguishing
factor of Salusin-β is its effect on blood pressure and vasodilation. While both Salusin-α and Salusin-β
have activities related to cardiovascular function, Salusin-β is more prominently involved in regulating
vasoconstriction and can influence systemic blood pressure more substantially. This potent action on
vascular tone primarily differentiates it from other similar peptides that have lesser effects on these
parameters. Salusin-β is known for being a potent hypotensive agent, meaning it can significantly lower
blood pressure, which might make it beneficial for therapeutic strategies against hypertension, a
prevalent condition linked to cardiovascular morbidity.
Salusin-β also plays a pivotal role in
influencing LDL and HDL cholesterol levels in human plasma, demonstrating its involvement in lipid
metabolism. This capacity to modulate plasma cholesterol profiles gives Salusin-β an added dimension of
interest in research focused on atherosclerosis and metabolic syndrome. This distinctive influence on
lipid profiles is not as pronounced in other peptides that only tangentially affect such parameters.
Moreover, Salusin-β’s interaction with various receptors at the cellular level and its involvement in
cell signaling pathways differentiates it further from peptides that may not engage with the same array
of cellular receptors or elicit the same biological responses.
Furthermore, Salusin-β has been
observed to have broader effects on the nervous and immune systems, with implications for modulation of
stress responses and inflammatory processes, making it a peptide of immense interest and research
potential. This wide-ranging impact on various physiological systems underscores the uniqueness of
Salusin-β relative to other related peptides, which may have more limited systemic effects.
How
does Salusin-β (human) interact with the cardiovascular system, and what are the implications of these
interactions?
Salusin-β (human) is a peptide known for its profound impacts on the cardiovascular
system, drawing interest from researchers aiming to dissect its potential therapeutic roles. One of the
primary interactions of Salusin-β with the cardiovascular system is its capacity to modulate vascular
tone. Salusin-β exerts potent vasodilatory effects, which consequently result in the widening of blood
vessels. This mechanism is crucial as it leads to a reduction in peripheral vascular resistance, thereby
lowering systemic blood pressure. Such hypotensive effects highlight Salusin-β as a potential
therapeutic candidate for managing hypertension, a condition affecting millions globally and being a
major risk factor for cardiovascular diseases.
The interaction of Salusin-β with the
cardiovascular system also involves its influence on myocardial contractility. Salusin-β has been shown
to enhance cardiac output by positively affecting the heart's contractile function. This characteristic
suggests that Salusin-β has a beneficial role in conditions characterized by compromised cardiac output,
such as heart failure. The ability of Salusin-β to improve myocardial efficiency and function represents
a key area of interest, potentially translating into therapeutic applications aimed at enhancing cardiac
output without adversely increasing heart rate or causing tachycardia.
Moreover, Salusin-β
influences lipid metabolism by modulating cholesterol levels, thereby affecting cardiovascular health
indirectly. By promoting favorable changes in lipid profiles, such as increasing HDL and reducing LDL
cholesterol, Salusin-β potentially helps mitigate atherosclerosis, a condition characterized by plaque
build-up in arteries leading to heart disease and stroke. This lipid-modulating property further
enhances the importance of Salusin-β in comprehensive cardiovascular health management, as dyslipidemia
is a critical factor contributing to cardiovascular complications.
Another crucial interaction of
Salusin-β with the cardiovascular system is its role in preventing endothelial dysfunction. The
endothelium, which is the inner lining of blood vessels, plays a pivotal role in maintaining vascular
health. Salusin-β has been noted to promote endothelial nitric oxide production, which is essential for
vasodilation and preventing thrombosis. These actions are crucial for preserving vascular health and
preventing complications such as arteriosclerosis and thrombosis. The endothelial supportive properties
of Salusin-β underscore its potential utility in preventing vascular complications often associated with
diabetes and hypertension.
Given these interactions, the implications of Salusin-β for
cardiovascular therapy are vast. Ongoing research is focused on elucidating the complete array of
mechanisms through which Salusin-β exerts these effects and confirming its safety and efficacy for
clinical applications. The aim is to harness its potential for developing novel therapeutics targeting
heart disease, high blood pressure, and related conditions. These promising cardiovascular benefits make
Salusin-β an exciting prospect in the field of cardiovascular research, with potential translational
applications that could revolutionize the management of cardiovascular diseases.
What role does
Salusin-β (human) play in the modulation of lipid metabolism?
Salusin-β (human) is intricately
involved in the modulation of lipid metabolism, showcasing its multifaceted role in human physiology
beyond its primary cardiovascular effects. Lipid metabolism encompasses the processes through which
lipids are synthesized, metabolized, transported, and utilized in the body, and Salusin-β plays a
significant role in these processes, providing critical insights into managing metabolic disorders that
are linked to lipid dysregulation, such as obesity, atherosclerosis, and metabolic syndrome.
One
of the primary roles of Salusin-β in lipid metabolism is its influence on cholesterol homeostasis.
Salusin-β has been noted to modulate the levels of circulating cholesterol, notably affecting
low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol. It promotes the
mobilization and clearance of LDL cholesterol, which is often referred to as "bad" cholesterol due to
its propensity to contribute to plaque formation in arteries. By reducing LDL cholesterol, Salusin-β
helps reduce the risk of atherosclerosis, thereby contributing to cardiovascular
health.
Additionally, Salusin-β may facilitate the increase of HDL cholesterol, known as "good"
cholesterol, which plays a crucial role in the reverse transport of cholesterol from peripheral tissues
back to the liver for excretion. This process is vital for maintaining a balanced lipid profile and
preventing the accumulation of excess cholesterol in arterial walls. Hence, Salusin-β, by promoting a
favorable lipid profile, significantly contributes to the reduction of atherosclerotic risk and the
promotion of cardiovascular wellness.
Salusin-β’s regulatory role in lipid metabolism extends to
its impact on fatty acid synthesis and oxidation within the liver. The liver is a central organ in lipid
metabolism, responsible for synthesizing and regulating fat levels in the body. By modulating hepatic
enzymes involved in lipid metabolism, Salusin-β influences the balance between fatty acid synthesis and
degradation, ensuring that lipid homeostasis is maintained. This regulatory effect on hepatic lipid
metabolism is crucial, given that imbalances in hepatic lipid handling are closely associated with
conditions such as non-alcoholic fatty liver disease (NAFLD) and hepatic steatosis.
Moreover,
Salusin-β may have a role in the adipose tissue's functionality, influencing lipid storage and
mobilization. This action contributes to energy homeostasis and possibly affects adipogenesis, which is
the process of forming new adipocytes, or fat cells. Proper functioning and regulation of adipose tissue
are paramount for preventing obesity and associated metabolic dysfunctions. By impacting the storage and
release of fatty acids in adipose tissue, Salusin-β potentially influences metabolic health and the
body's ability to manage energy efficiently.
In summary, Salusin-β’s ability to modulate various
aspects of lipid metabolism positions it as a valuable target for research into metabolic disorders. By
influencing cholesterol levels, hepatic lipid synthesis and oxidation, and adipose tissue function,
Salusin-β offers promising avenues for therapeutic strategies aimed at managing and potentially treating
metabolic and cardiovascular diseases linked to lipid dysregulation.
How does Salusin-β (human)
affect cellular function, particularly in terms of receptor interaction and signaling
pathways?
Salusin-β (human) is a peptide that plays significant roles in cellular function,
particularly through its complex interplay with cellular receptors and subsequent activation or
inhibition of various signaling pathways. These interactions underline the peptide's functional
versatility and the breadth of its physiological impact, emphasizing its regulatory potential across
different bodily systems.
One of the primary aspects of Salusin-β’s effect on cellular function
is its interaction with G-protein-coupled receptors (GPCRs). GPCRs are a large family of cell surface
receptors involved in transmitting signals from external stimuli into cells, subsequently activating
intracellular signaling cascades that initiate specific cellular responses. Salusin-β can bind to GPCRs,
influencing signaling pathways that regulate a variety of physiological processes. For instance, its
binding can lead to the activation of adenylate cyclase, an enzyme that catalyzes the conversion of ATP
to cyclic AMP (cAMP), a secondary messenger involved in regulating numerous cellular processes such as
metabolism, gene transcription, and cell proliferation.
Salusin-β also influences cellular
function through its role in modulating intracellular calcium levels. Calcium ions act as crucial
secondary messengers in many signaling pathways, and Salusin-β can affect calcium influx by acting on
voltage-gated calcium channels or through receptor-mediated mechanisms. This modulation of calcium
levels is vital for various cellular activities, including muscle contraction, neurotransmitter release,
and cellular apoptosis. By influencing calcium signaling, Salusin-β exerts significant control over
processes such as vascular tone regulation, which is vital for maintaining proper cardiovascular
function.
Moreover, Salusin-β can affect kinase signaling cascades, such as those involving
protein kinase C (PKC) and mitogen-activated protein kinases (MAPKs). These kinase pathways are integral
to mediating cellular responses to stress, growth factors, and other stimuli. The activation of PKC and
MAPKs by Salusin-β can lead to changes in cell proliferation, differentiation, and apoptosis, processes
crucial for tissue growth, repair, and homeostasis. The involvement in these pathways suggests potential
implications of Salusin-β in cancer biology, as dysregulated cell growth and apoptosis are hallmarks of
cancerous transformation.
Salusin-β’s ability to modulate nitric oxide (NO) signaling also
exemplifies its impact on cellular functions. NO is a critical signaling molecule in vascular biology,
affecting vasodilation, blood pressure regulation, and endothelial function. By influencing NO
production and signaling, Salusin-β contributes to the maintenance of vascular homeostasis and
prevention of vascular-related diseases. The regulation of NO signaling embodies Salusin-β’s potential
utility in therapeutic contexts, particularly for cardiovascular diseases characterized by endothelial
dysfunction and impaired vasodilation.
Overall, Salusin-β’s interactions with cellular receptors
and its influence on various signaling pathways highlight the peptide’s multifaceted role in cellular
function. Its ability to modulate GPCR-mediated signaling, calcium influx, kinase activation, and NO
production encapsulates its systemic impact, with significant implications for health and disease. These
diverse interactions illustrate Salusin-β’s potential as a pharmacological target, offering pathways for
developing new treatments for metabolic, cardiovascular, and possibly oncological diseases.
What
implications does Salusin-β (human) have for metabolic health and disorders like
diabetes?
Salusin-β (human) is garnering considerable attention for its implications in metabolic
health, particularly concerning chronic disorders such as diabetes. Diabetes, characterized by high
blood sugar levels and associated with several metabolic disturbances, represents a major public health
challenge worldwide. Salusin-β's involvement in key physiological processes offers insight into its
potential roles in mitigating or managing diabetes and associated metabolic derangements.
One
significant aspect of Salusin-β’s role in metabolic health relates to its influence on glucose
metabolism. Salusin-β has been observed to affect insulin sensitivity, a crucial factor in glucose
homeostasis. Enhanced insulin sensitivity allows cells to more effectively utilize glucose, thereby
reducing hyperglycemia, a hallmark of diabetes. Salusin-β’s ability to improve insulin action could
translate into better glycemic control, potentially offering therapeutic strategies to manage type 2
diabetes, characterized by insulin resistance.
Beyond glucose metabolism, Salusin-β impacts lipid
metabolism, which is often disrupted in metabolic disorders like diabetes. As mentioned earlier,
Salusin-β modulates cholesterol levels and influences hepatic lipid synthesis. These actions can
contribute to improved lipid profiles and overall metabolic balance. Dyslipidemia, an aberration in
lipid levels, often accompanies diabetes, exacerbating cardiovascular risk. By influencing lipid
metabolism, Salusin-β could help in managing this aspect of diabetes, thus reducing cardiovascular
complications associated with the disease.
Furthermore, Salusin-β plays a role in regulating
inflammatory pathways. Chronic inflammation is well-recognized in the pathogenesis of insulin resistance
and type 2 diabetes. Salusin-β’s ability to modulate the immune response and downregulate
pro-inflammatory cytokine production presents a mechanism by which it could ameliorate inflammatory
states associated with metabolic disorders. Controlling inflammation through Salusin-β could lead to
improved metabolic health and reduced progression of diabetes-related complications.
Salusin-β’s
role in cell signaling also underlines its impact on pancreatic β-cell function, which is critical in
diabetes pathophysiology. Salusin-β may influence β-cell survival and functionality, thereby affecting
insulin secretion. Preserving β-cell mass and function is foundational in diabetes management,
especially in type 1 diabetes and advanced type 2 diabetes cases where β-cell failure predominates. By
supporting β-cell health, Salusin-β potentially contributes to sustained insulin production and
secretion, aiding in better long-term management of blood glucose levels.
Additionally, Salusin-β
could affect energy expenditure and adiposity, factors related to the development and progression of
obesity and its complications like diabetes. Its potential role in adipocyte function and regulation of
metabolic rate underscores its multifaceted impact on energy balance, an essential component in managing
obesity-related diabetes.
Research efforts continue to explore Salusin-β’s full potential in
metabolic health and its translational applicability in treating metabolic disorders like diabetes. By
elucidating the precise mechanisms and effects of Salusin-β, further advances could be made in using it
as part of strategic interventions aimed at overcoming the metabolic challenges posed by diabetes. As
such, Salusin-β stands out as a promising candidate in the quest for innovative therapeutic solutions in
metabolic medicine.