20% off purchase of 3 or more products* | Learn More >>

Polyclonal Antibody Cell Volume Homeostasis

Also showing Polyclonal Antibody Immunoprecipitation Cell Volume Homeostasis, Polyclonal Antibody Western Blotting Cell Volume Homeostasis

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse, Rat

Application Methods: Immunoprecipitation, Western Blotting

Background: Leucine-rich repeat containing 8 family member A (LRRC8A) belongs to the leucine-rich repeat family of proteins. It is also named SWELL1. LRRC8A forms a heteromeric complex called the volume regulated anion channel (VRAC) with other family members such as LRRC8B, LRRC8C, LRRC8D, or LRRC8E. VRAC maintains cell volume in response to extracellular or intracellular osmotic changes (1,2). The LRRC8A-containing VRAC complex senses ionic strength and is activated by hypotonic stress (3). LRRC8A is also involved in B cell development. Mutations in the LRRC8A gene causes agammaglobulinemia, which is a primary immunodeficiency characterized by severely low or absent serum antibodies and circulating B-cells (4).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse, Rat

Application Methods: Immunoprecipitation, Western Blotting

Background: The Na-K-2Cl cotransporter (NKCC2) is a sodium-potassium-chloride cotransporter. It is mainly expressed on the luminal membrane of renal epithelial cells of the thick ascending limb of Henle's loop (TALH) and mediates the majority of NaCl resorption and concentration of urine (1,2). NKCC2 is the target for several diuretic drugs, such as bumetanide, and is involved in the pathogenesis of hypertension (3,4). Mutations in the NKCC2-encoding gene, SLC12A1, causes Bartter’s syndrome, which is featured by impaired salt reabsorption in the TALH, hypokalemic metabolic alkalosis, and hypercalciuria (5,6). Recently, NKCC2 was reported to be expressed in the brain hypothalamo-neurohypophyseal system (HNS) and upregulated upon osmotic stress (7).

$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Immunoprecipitation, Western Blotting

Background: The electroneutral cation-chloride-coupled co-transporter (SLC12) gene family comprises bumetanide-sensitive Na+/K+/Cl- (NKCC), thiazide-sensitive Na+/Cl-, and K+/Cl- (KCC) co-transporters. SLC12A1/NKCC2 and SLC12A2/NKCC1 regulate cell volume and maintain cellular homeostasis in response to osmotic and oxidative stress (1). The broadly expressed NKCC1 is thought to play roles in fluid secretion (i.e. salivary gland function), salt balance (i.e. maintenance of renin and aldosterone levels), and neuronal development and signaling (2-7). During neuronal development, NKCC1 and KCC2 maintain a fine balance between chloride influx (NKCC1) and efflux (KCC2), which regulates γ-aminobutyric acid (GABA)-mediated neurotransmission (3). Increased NKCC1 expression in immature neurons maintains high intracellular chloride levels that result in inhibitory GABAergic signaling; KCC2 maintains low intracellular chloride levels and excitatory GABAergic responses in mature neurons (4,5,8). Deletion of NKCC1 impairs NGF-mediated neurite outgrowth in PC-12D cells while inhibition of NKCC1 with bumetanide inhibits re-growth of axotomized dorsal root ganglion cells (6,7). Defective chloride homeostasis in neurons is linked to seizure disorders that are ameliorated by butemanide treatment, indicating that abnormal NKCC1 and NKCC2 expression or signaling may play a role in neonatal and adult seizures (9-12). NKCC1 is found as a homodimer or within heterooligomers with other SLC12 family members. This transport protein associates with a number of oxidative- and osmotic-responsive kinases that bind, phosphorylate, and activate NKCC1 co-transporter activity (13-16). In response to decreased intracellular chloride concentrations, Ste20-related proline-alanine-rich kinase (SPAK) phosphorylates NKCC1 to increase co-transporter activity and promote chloride influx (16-19). Oxidative stress response kinase 1 (OSR1) also phosphorylates and activates NKCC1 in response to oxidative stress (14).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey

Application Methods: Immunoprecipitation, Western Blotting

Background: TRPV4 is a member of the transient receptor potential vanilloid (TRPV) family of ion channels, and functions as a Ca2+-permeant non-selective cation channel. TRPV4 channels are expressed in many cell types, with particular abundance in sensory and spinal neurons (1). TRPV4 channels play a role in maintaining cellular homeostasis, by facilitating transmembrane Ca2+ transport in response to various stimuli, including thermal stress, fatty acid metabolites, and hypotonicity (2). Mutations in the TRPV4 gene have consequently been attributed to a variety of pathological conditions. For example, constitutively active TRPV4 mutants can lead to excess Ca2+ influx, resulting in toxicity and degeneration of peripheral nerves (3). TRPV4-dependent Ca2+ influx was also shown to mediate strain-induced and TGFβ1-induced epithelial-mesenchymal transition (EMT), suggesting a mechanistic role for TRPV4-mediated Ca2+ transport in fibrosis and oncogenesis (4). Consistent with this, studies in capillary endothelial cells showed that mechanical strain-induced Ca2+ influx through TRPV4 promote focal adhesion and stress fiber remodeling, mediated specifically through integrins, PI3K, and downstream kinases including Rho and ROCK (5).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse

Application Methods: Immunoprecipitation, Western Blotting

Background: Angiotensinogen (AGT) is the primary precursor of angiotensins, peptide hormones that play a central role in the renin-angiotensin system (RAS) (1-3). AGT is a secreted protein synthesized primarily by the liver and secreted into circulation. Upon binding to renin, the amino terminal fragment of AGT is cleaved and released as a decapeptide hormone termed angiotensin 1 (Ang I). Ang I is subsequently processed by angiotensin converting enzyme (ACE) to generate angiotensin II (Ang II), which acts on AT1 and AT2 receptors in the central nervous system to increase production of anti-diuretic hormone (ADH), while promoting vasoconstriction in the peripheral circulation (4). Aberrant upregulation of Ang II has been associated with numerous clinical conditions, including hypertension, atherosclerosis, myocardial hypertrophy, and obesity (5-7). Alternative cleavage products of Ang I (e.g., Ang 1-7) can also be generated by ACE2 cleavage, some of which display biological functions that are distinct from Ang II (8). Treatments that target the RAS (e.g., ACE inhibitors) are consequently of significant importance in the treatment of hypertensive and hypertensive-related disorders(5-8).