Cell state · L2
PLAT.megakaryocytic
135 cells in the full atlas (not the displayed sample).
These are the cell-population annotations shown in the SCREATE Cell Browser.
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Marker genes
AKIRIN2, CCNG1, CFLAR, ELF1, FAM110A, GATA1, GMFG, HEMGN, HHEX, IFRD1, KCNA3, LGALS12, LYL1, MAP4K5, NFE2, NT5C3A, PCYT1B, PSTPIP2, QKI, RAB27B, RAB32, RAP2B, RASGRP2, RBM38, RGS3, SEC14L1, SMOX, SNHG7, SSX2IP, TECPR2, TMEM140, TSC22D1, TXNL4B, UBALD2
Annotation genes
GATA1, NFE2, RAB27B, RAP2B, RASGRP2
Annotation rationales
Presence of lineage-defining transcription factors GATA1, NFE2, HHEX, LYL1, and HEMGN reveals residual megakaryocyte imprint in this platelet cluster. Alongside this, vesicle trafficking machinery (RAB27B, RAP2B, RASGRP2) underscores robust capacity for dense- and α-granule release. CCNG1 and CFLAR suggest stress/adaptive readiness, while signaling adaptors (RGS3, MAP4K5) fine-tune platelet activation thresholds. This places the cluster transcriptionally closer to its precursor megakaryocytes while retaining platelet functionality.
Functional implications
Functions as a highly secretory and signaling-competent platelet subset, primed for strong granule exocytosis during thrombus formation. By retaining megakaryocyte-driven transcriptional programs, these platelets excel in orchestrating vascular repair, fibrin stabilization, and immune–vascular crosstalk. In the immune system, they act as sentinels that deploy chemokines and growth factors from α-granules (e.g., PF4, VEGF, TGF-β, not in marker set but functionally implied) to recruit leukocytes, stimulate endothelial remodeling, and bridge innate immunity with hemostatic repair.
Marker and functional descriptions are atlas annotations. Explore gene expression, trait associations and regulatory elements in the interactive browsers; see the browser guide.