KRIM-1 Inhibitors
Chemical inhibitors of KRIM-1 encompass a range of compounds that target various signaling pathways and cellular processes, each with the potential to modulate the activity of KRIM-1 through different mechanisms. Palbociclib, for instance, can alter the function of KRIM-1 by inducing cell cycle arrest at the G1 phase, which is likely to downregulate proteins dependent on cell cycle progression. Similarly, the mTOR pathway, a central player in cell growth and proliferation, can be inhibited by Rapamycin. This inhibition can decrease the activity of proteins such as KRIM-1 if they are part of or regulated by this pathway. The PI3K/AKT pathway, another crucial signaling axis for cell survival and metabolism, can be inhibited by LY294002 and Wortmannin, which can in turn decrease the functional activity of KRIM-1. Triciribine further extends this inhibition specifically to the AKT kinase, directly reducing the activation and potentially the activity of KRIM-1.
In addition to inhibitors targeting growth and proliferation pathways, compounds like U0126 and PD98059 can functionally inhibit KRIM-1 by preventing the activation of the ERK pathway, a key signaling route that can regulate a variety of cellular responses, possibly including those associated with KRIM-1. SB203580 and SP600125 offer a more stress response-oriented inhibition, targeting p38 MAPK and JNK, respectively. By inhibiting these kinases, the inhibitors can reduce the functional activity of KRIM-1 if it is involved in pathways responsive to stress signals or apoptosis. Bortezomib's proteasome inhibition can lead to the accumulation of regulatory proteins that may inhibit KRIM-1 activity if it is subject to proteasomal degradation. Finally, ZM447439 and Sunitinib act on cell division and receptor tyrosine kinases, respectively; ZM447439 by inhibiting Aurora kinases, which are critical during mitosis, and Sunitinib by targeting RTKs, which could inhibit KRIM-1 if it relies on these for signaling. Together, these chemical inhibitors cover a broad spectrum of cellular mechanisms, each with the capacity to modulate the activity of KRIM-1 through distinct but potentially overlapping pathways.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Palbociclib | 571190-30-2 | sc-507366 | 50 mg | $315.00 | ||
Palbociclib is a selective inhibitor of cyclin-dependent kinases CDK4 and CDK6. KRIM-1, being a protein influenced by cell cycle regulation, would be functionally inhibited as Palbociclib-induced cell cycle arrest in the G1 phase would result in downregulation of proteins that are dependent on cell cycle progression for their activity or stability. | ||||||
Rapamycin | 53123-88-9 | sc-3504 sc-3504A sc-3504B | 1 mg 5 mg 25 mg | $62.00 $155.00 $320.00 | 233 | |
Rapamycin is an mTOR inhibitor, and mTOR is a central regulator of cell growth and proliferation. By inhibiting the mTOR pathway, Rapamycin can decrease the activity of downstream effectors that are essential for the function of proteins such as KRIM-1, which may be involved in cellular growth and metabolic processes. | ||||||
LY 294002 | 154447-36-6 | sc-201426 sc-201426A | 5 mg 25 mg | $121.00 $392.00 | 148 | |
LY294002 is a potent inhibitor of phosphatidylinositol 3-kinase (PI3K). Since PI3K signaling is crucial for a multitude of cellular functions, including those that may involve KRIM-1, inhibition of this pathway by LY294002 could lead to a decrease in KRIM-1 activity due to reduced signaling through the AKT pathway, which is downstream of PI3K. | ||||||
U-0126 | 109511-58-2 | sc-222395 sc-222395A | 1 mg 5 mg | $63.00 $241.00 | 136 | |
U0126 is an inhibitor of MEK1/2, which are upstream activators of the ERK pathway. Inhibition of this pathway can lead to a reduction in the activity of downstream proteins that are regulated by ERK signaling. Since KRIM-1 may be influenced by the ERK pathway, U0126 can functionally inhibit KRIM-1 by reducing ERK-mediated cellular responses. | ||||||
SB 203580 | 152121-47-6 | sc-3533 sc-3533A | 1 mg 5 mg | $88.00 $342.00 | 284 | |
SB203580 is a well-known p38 MAPK inhibitor. The p38 MAPK pathway is involved in the response to stress stimuli and inflammation. Inhibition of p38 MAPK by SB203580 can lead to the functional inhibition of KRIM-1 if KRIM-1 is involved in pathways that are responsive to stress and inflammatory signals mediated by p38 MAPK. | ||||||
SP600125 | 129-56-6 | sc-200635 sc-200635A | 10 mg 50 mg | $40.00 $150.00 | 257 | |
SP600125 is an inhibitor of c-Jun N-terminal kinase (JNK). JNKs are part of the MAP kinase family and are involved in controlling gene expression and cellular apoptosis. By inhibiting JNK, SP600125 could decrease the functional activity of KRIM-1 if it is regulated by or dependent on JNK signaling for its activity. | ||||||
PD 98059 | 167869-21-8 | sc-3532 sc-3532A | 1 mg 5 mg | $39.00 $90.00 | 212 | |
PD98059 acts as a specific inhibitor of MEK, which prevents the activation of ERK. If KRIM-1 is functionally regulated by the ERK pathway, PD98059 would inhibit the activity of KRIM-1 by preventing its activation or expression as a result of the inhibition of ERK signaling. | ||||||
Wortmannin | 19545-26-7 | sc-3505 sc-3505A sc-3505B | 1 mg 5 mg 20 mg | $66.00 $219.00 $417.00 | 97 | |
Wortmannin is a potent inhibitor of PI3K. Similar to LY294002, wortmannin can functionally inhibit KRIM-1 by blocking the PI3K/AKT signaling pathway, which might control processes that KRIM-1 is involved in, such as cell survival, proliferation, and metabolism. | ||||||
Triciribine | 35943-35-2 | sc-200661 sc-200661A | 1 mg 5 mg | $102.00 $138.00 | 14 | |
Triciribine specifically inhibits the activation of AKT. By preventing AKT activation, triciribine could functionally inhibit KRIM-1 if the activity or stability of KRIM-1 is dependent on AKT-mediated signaling pathways. | ||||||
Bortezomib | 179324-69-7 | sc-217785 sc-217785A | 2.5 mg 25 mg | $132.00 $1064.00 | 115 | |
Bortezomib is a proteasome inhibitor that can disrupt the degradation of cell cycle and apoptosis regulatory proteins. If KRIM-1 is regulated by proteasomal degradation, bortezomib could lead to an accumulation of regulatory proteins that could inhibit the function of KRIM-1. | ||||||