Btnl6, or Butyrophilin-like 6, emerges as a key player in cellular regulation, with a predicted function centered around signaling receptor binding activity and involvement in extrathymic T cell selection. The predicted role of Btnl6 as a signaling receptor binder implies its engagement in cellular communication processes, possibly facilitating interactions between cells. This suggests a potential role for Btnl6 in mediating immune responses or other cellular functions where signaling is crucial. The connection of Btnl6 to extrathymic T cell selection adds another layer to its significance, indicating a part in shaping the immune system's repertoire outside the thymus. The orthologous relationship with human BTNL3 and BTNL8 suggests evolutionary conservation of functions, emphasizing the importance of Btnl6 across species. The activation of Btnl6 involves intricate interactions with various signaling pathways and cellular processes. The identified chemicals, acting either directly or indirectly, provide insights into the diverse mechanisms influencing Btnl6 expression. For instance, retinoic acid indirectly activates Btnl6 by modulating the retinoic acid signaling pathway, suggesting a link between Btnl6 and retinoic acid-mediated immune regulation. Additionally, forskolin indirectly activates Btnl6 through the cAMP-dependent pathway, shedding light on its potential involvement in cellular responses associated with elevated cAMP levels.
The interconnectedness with TGF-β, JAK-STAT, PPARγ, MAPK, PI3K/Akt, NF-κB, and Wnt/β-catenin signaling pathways further underscores Btnl6's adaptability and its ability to integrate signals from diverse cellular environments. These mechanisms collectively highlight Btnl6's versatility in cellular regulation, positioning it as a pivotal player in orchestrating cellular responses and influencing extrathymic T cell selection. In conclusion, Btnl6 emerges as a multifaceted gene with a predicted function in signaling receptor binding activity and a role in extrathymic T cell selection. Its activation involves intricate crosstalk with various signaling pathways, suggesting its adaptability and responsiveness to diverse cellular cues. The identified chemicals provide a glimpse into the complex regulatory network governing Btnl6 expression, offering valuable insights into its role in cellular communication and immune system modulation. Understanding Btnl6 and its activation mechanisms contributes to unraveling the intricate web of cellular processes, furthering our knowledge of immune regulation and cellular responses.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Retinoic Acid, all trans | 302-79-4 | sc-200898 sc-200898A sc-200898B sc-200898C | 500 mg 5 g 10 g 100 g | $66.00 $325.00 $587.00 $1018.00 | 28 | |
Retinoic acid indirectly activates Btnl6 by influencing the retinoic acid signaling pathway. Retinoic acid receptors (RARs) bind to Btnl6 regulatory elements, modulating its expression and contributing to extrathymic T cell selection. This suggests a role for Btnl6 in retinoic acid-mediated immune regulation. | ||||||
SB 203580 | 152121-47-6 | sc-3533 sc-3533A | 1 mg 5 mg | $90.00 $349.00 | 284 | |
p38 MAPK inhibitor influencing Btnl6 indirectly. By inhibiting p38 MAPK, it modulates downstream signaling. Btnl6, predicted to enable signaling receptor binding activity, may be indirectly activated through altered p38 MAPK-dependent pathways, influencing processes related to signaling receptor binding and cellular activation. | ||||||
JAK Inhibitor I | 457081-03-7 | sc-204021 sc-204021A | 500 µg 1 mg | $156.00 $339.00 | 59 | |
JAK Inhibitor I indirectly activates Btnl6 by inhibiting JAK-STAT signaling. This interference leads to altered Btnl6 expression, indicating its potential role in signaling receptor binding activity and influencing extrathymic T cell selection mechanisms associated with JAK-STAT pathways. | ||||||
GW 9662 | 22978-25-2 | sc-202641 | 5 mg | $70.00 | 30 | |
As a PPARγ antagonist, GW9662 indirectly activates Btnl6 by influencing PPARγ signaling. This modulation impacts Btnl6 expression, suggesting its involvement in signaling receptor binding activity and providing insights into extrathymic T cell selection mechanisms associated with PPARγ pathways. | ||||||
PD 169316 | 152121-53-4 | sc-204168 sc-204168A sc-204168B sc-204168C | 1 mg 5 mg 10 mg 25 mg | $88.00 $156.00 $281.00 $461.00 | 3 | |
p38 MAPK inhibitor influencing Btnl6 indirectly. By inhibiting p38 MAPK, it modulates downstream signaling. Btnl6, predicted to enable signaling receptor binding activity, may be indirectly activated through altered p38 MAPK-dependent pathways, influencing processes related to signaling receptor binding and cellular activation. | ||||||
LY 303511 | 154447-38-8 | sc-202215 sc-202215A | 1 mg 5 mg | $67.00 $278.00 | 3 | |
PI3K inhibitor indirectly impacting Btnl6. By inhibiting PI3K, it modulates downstream signaling. Btnl6, predicted to enable signaling receptor binding activity, may be indirectly activated through altered PI3K-dependent pathways, influencing processes related to signaling receptor binding and cellular activation. | ||||||
AZD8055 | 1009298-09-2 | sc-364424 sc-364424A | 10 mg 50 mg | $163.00 $352.00 | 12 | |
mTOR inhibitor impacting Btnl6 indirectly. By inhibiting mTOR, it modulates downstream signaling. Btnl6, involved in extrathymic T cell selection, may be indirectly activated through altered mTOR-dependent pathways, influencing processes related to T cell selection and immune response. | ||||||
Ampeloptin | 27200-12-0 | sc-480419 | 10 mg | $300.00 | ||
JNK inhibitor affecting Btnl6 indirectly. By inhibiting JNK, it modulates downstream signaling. Btnl6, predicted to enable signaling receptor binding activity, may be indirectly activated through altered JNK-dependent pathways, influencing processes related to signaling receptor binding and cellular activation. | ||||||