Morf4l1b, identified as a mortality factor 4 like 1B, emerges as a pivotal player in cellular processes associated with condensed mesenchymal cell proliferation and nephron development. Predicted to engage in calcium ion binding activity and exhibit activity in cell-cell junctions, Morf4l1b's multifaceted role extends to crucial developmental events within tissues like the brain, pharyngo-tympanic tube, and spinal cord. This protein's orthology to the human DCHS2 highlights its evolutionary significance, suggesting conserved functions across species. The function of Morf4l1b centers on its involvement in calcium ion binding and subsequent regulation of cell-cell junctions, positioning it at critical points in condensed mesenchymal cell proliferation and nephron development. The disruption of Morf4l1b's activity necessitates a nuanced approach, involving both direct and indirect inhibition. The presented chemicals target Morf4l1b through diverse mechanisms. For instance, calcium ion binding inhibitors directly interfere with Morf4l1b's role by disrupting its calcium coordination, impairing cell-cell junction dynamics and affecting mesenchymal cell proliferation during nephrogenesis.
Additionally, indirect inhibition through modulators of pathways such as mTOR, TGF-β, PI3K/Akt, and Wnt illustrates the intricate web of interconnected signaling cascades that influence Morf4l1b's function. These modulators disrupt downstream events, impacting Morf4l1b-related functions and contributing to the regulation of cell-cell interactions and developmental processes. The varied mechanisms of inhibition underscore the complexity of cellular regulation, highlighting the need for a detailed understanding of the interconnected pathways that govern Morf4l1b's activities. In conclusion, Morf4l1b plays a crucial role in orchestrating cellular processes integral to development. Its inhibition, whether direct or indirect, involves a sophisticated interplay of biochemical and cellular pathways. The disruption of calcium ion binding, coupled with the modulation of key signaling pathways, collectively contributes to the nuanced regulation of Morf4l1b's functions. Understanding these intricate interactions sheds light not only on the specific role of Morf4l1b but also on the broader regulatory networks governing fundamental cellular processes. This comprehensive perspective is crucial for advancing our knowledge in developmental biology and cellular dynamics.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Nifedipine | 21829-25-4 | sc-3589 sc-3589A | 1 g 5 g | $58.00 $170.00 | 15 | |
Nifedipine inhibits Morf4l1b by interfering with its calcium ion binding activity. This disruption negatively impacts the protein's role in condensed mesenchymal cell proliferation and nephron development, consequently influencing cell-cell junction dynamics. | ||||||
Rapamycin | 53123-88-9 | sc-3504 sc-3504A sc-3504B | 1 mg 5 mg 25 mg | $62.00 $155.00 $320.00 | 233 | |
Rapamycin indirectly inhibits Morf4l1b by targeting the mTOR pathway. By inhibiting mTOR, rapamycin disrupts downstream events, impacting Morf4l1b-related functions in cell-cell junction and mesenchymal cell proliferation during nephron development. | ||||||
SB 431542 | 301836-41-9 | sc-204265 sc-204265A sc-204265B | 1 mg 10 mg 25 mg | $80.00 $212.00 $408.00 | 48 | |
SB-431542 acts as a TGF-β receptor inhibitor, indirectly affecting Morf4l1b. By blocking the TGF-β signaling pathway, SB-431542 disrupts downstream events, interfering with Morf4l1b's role in cell-cell junction and mesenchymal cell proliferation during nephron development. | ||||||
Thapsigargin | 67526-95-8 | sc-24017 sc-24017A | 1 mg 5 mg | $94.00 $349.00 | 114 | |
Thapsigargin inhibits Morf4l1b indirectly by disrupting calcium homeostasis. As a sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) inhibitor, thapsigargin induces calcium release imbalance, impacting Morf4l1b's calcium ion binding activity and subsequently hindering its cellular functions. | ||||||
LY 294002 | 154447-36-6 | sc-201426 sc-201426A | 5 mg 25 mg | $121.00 $392.00 | 148 | |
LY294002, a PI3K inhibitor, indirectly influences Morf4l1b by disrupting the PI3K/Akt signaling pathway. This interference leads to downstream effects that negatively impact Morf4l1b's role in cell-cell junction and mesenchymal cell proliferation during nephron development. | ||||||
PD 98059 | 167869-21-8 | sc-3532 sc-3532A | 1 mg 5 mg | $39.00 $90.00 | 212 | |
PD98059, a MEK inhibitor, indirectly influences Morf4l1b by disrupting the MAPK/ERK signaling pathway. This interference leads to downstream effects that negatively impact Morf4l1b's role in cell-cell junction and mesenchymal cell proliferation during nephron development. | ||||||
SB 203580 | 152121-47-6 | sc-3533 sc-3533A | 1 mg 5 mg | $88.00 $342.00 | 284 | |
SB-203580, a p38 MAPK inhibitor, indirectly influences Morf4l1b by disrupting the p38 MAPK signaling pathway. This interference leads to downstream effects that negatively impact Morf4l1b's role in cell-cell junction and mesenchymal cell proliferation during nephron development. | ||||||
A-769662 | 844499-71-4 | sc-203790 sc-203790A sc-203790B sc-203790C sc-203790D | 10 mg 50 mg 100 mg 500 mg 1 g | $180.00 $726.00 $1055.00 $3350.00 $5200.00 | 23 | |
A769662, an AMPK activator, indirectly influences Morf4l1b by modulating cellular energy balance. By activating AMPK, A769662 impacts downstream events that negatively impact Morf4l1b's role in cell-cell junction and mesenchymal cell proliferation during nephron development. | ||||||
MG-132 [Z-Leu- Leu-Leu-CHO] | 133407-82-6 | sc-201270 sc-201270A sc-201270B | 5 mg 25 mg 100 mg | $56.00 $260.00 $980.00 | 163 | |
MG-132, a proteasome inhibitor, indirectly influences Morf4l1b by disrupting the proteasomal degradation pathway. This interference leads to an accumulation of Morf4l1b, negatively impacting its role in cell-cell junction and mesenchymal cell proliferation during nephron development. | ||||||
GSK-3 Inhibitor XVI | 252917-06-9 | sc-221691 sc-221691A | 5 mg 25 mg | $153.00 $520.00 | 4 | |
GSK-3 Inhibitor XVI indirectly influences Morf4l1b by modulating the Wnt signaling pathway. By inhibiting GSK-3, CHIR-99021 disrupts downstream events, affecting Morf4l1b-related functions in cell-cell junction and mesenchymal cell proliferation during nephron development. | ||||||