ANK-1 inhibitors are a class of chemical compounds designed to target and modulate the activity of a specific protein known as Ankyrin-1 (ANK-1). Ankyrins are a family of adaptor proteins that play a crucial role in cell membrane stability and the organization of integral membrane proteins. ANK-1, in particular, is found in red blood cells (erythrocytes) and is essential for maintaining the structural integrity of the erythrocyte membrane. It functions as a bridge between the cell membrane and the underlying cytoskeleton, facilitating the attachment of important membrane proteins such as the anion exchanger (band 3) and the glucose transporter (GLUT1). These interactions are vital for maintaining the shape, flexibility, and overall functionality of red blood cells.
ANK-1 inhibitors are designed to interfere with the binding or activity of ANK-1, which can have significant implications for erythrocyte health and function. By targeting ANK-1, these inhibitors may disrupt the normal interactions between ANK-1 and membrane proteins, potentially leading to alterations in membrane stability, shape, and deformability. These effects could impact the ability of red blood cells to traverse narrow capillaries and fulfill their crucial role in oxygen transport throughout the body. The development and study of ANK-1 inhibitors have primarily focused on understanding the molecular mechanisms underlying erythrocyte membrane stability, with potential implications for diseases characterized by erythrocyte membrane defects. Additionally, ANK-1 inhibitors may hold promise in furthering our understanding of the broader roles of ankyrins in various cell types beyond erythrocytes.
SEE ALSO...
| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Sulfasalazine | 599-79-1 | sc-204312 sc-204312A sc-204312B sc-204312C | 1 g 2.5 g 5 g 10 g | $61.00 $77.00 $128.00 $209.00 | 8 | |
Sulfasalazine inhibits ANK-1 by disrupting the formation of the ANK-1/tubulin complex, leading to destabilization of the cytoskeleton. | ||||||
Phalloidin | 17466-45-4 | sc-202763 | 1 mg | $234.00 | 33 | |
Phalloidin inhibits ANK-1 by binding to and stabilizing F-actin filaments, preventing ANK-1 from interacting with the cytoskeleton. | ||||||
Cytochalasin D | 22144-77-0 | sc-201442 sc-201442A | 1 mg 5 mg | $165.00 $486.00 | 64 | |
Cytochalasin D disrupts ANK-1 by inhibiting actin polymerization, leading to impaired ANK-1 binding to the cytoskeleton. | ||||||
CK 666 | 442633-00-3 | sc-361151 sc-361151A | 10 mg 50 mg | $321.00 $1040.00 | 5 | |
CK-666 inhibits ANK-1 by blocking actin filament polymerization, preventing ANK-1 from interacting with the cytoskeleton. | ||||||
Latrunculin A, Latrunculia magnifica | 76343-93-6 | sc-202691 sc-202691B | 100 µg 500 µg | $265.00 $815.00 | 36 | |
Latrunculin A disrupts ANK-1 by sequestering actin monomers, preventing their incorporation into the cytoskeleton and ANK-1 binding. | ||||||
Jasplakinolide | 102396-24-7 | sc-202191 sc-202191A | 50 µg 100 µg | $184.00 $305.00 | 59 | |
Jasplakinolide inhibits ANK-1 by stabilizing F-actin filaments, preventing ANK-1 from dissociating from the cytoskeleton. | ||||||
Nocodazole | 31430-18-9 | sc-3518B sc-3518 sc-3518C sc-3518A | 5 mg 10 mg 25 mg 50 mg | $59.00 $85.00 $143.00 $247.00 | 38 | |
Nocodazole inhibits ANK-1 by depolymerizing microtubules, disrupting ANK-1 interactions with the microtubule network. | ||||||
(±)-Blebbistatin | 674289-55-5 | sc-203532B sc-203532 sc-203532A sc-203532C sc-203532D | 5 mg 10 mg 25 mg 50 mg 100 mg | $183.00 $313.00 $464.00 $942.00 $1723.00 | 7 | |
Blebbistatin inhibits ANK-1 by selectively disrupting the contractile function of nonmuscle myosin II, altering cytoskeletal dynamics. | ||||||
CK-869 | 388592-44-7 | sc-507274 | 5 mg | $163.00 | ||
CK-869 inhibits ANK-1 by interfering with actin dynamics, preventing ANK-1 from binding to and stabilizing the cytoskeleton. | ||||||
SMIFH2 | 340316-62-3 | sc-507273 | 5 mg | $140.00 | ||
SMIFH2 inhibits ANK-1 by disrupting formin-mediated actin polymerization, leading to reduced ANK-1 interactions with actin filaments. | ||||||