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Details for anatomical structure: hematopoietic stem cell

EndoNet ID: ENC00318

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hematopoietic stem cell, ,

General information

Hematopoietic stem cells (HSCs) are multipotent stem cells that give rise to all the blood cell types from the myeloid (monocytes and macrophages, neutrophils, basophils, eosinophils, erythrocytes, megakaryocytes/platelets, dendritic cells), and lymphoid lineages (T-cells, B-cells, NK-cells).

Links to other resources

Cytomer cy0052329

Larger structures


      Secreted hormones

      • Hormone: RANKL

        • PTH and VD3 (calcitriol) increase the expression of RANKL on the surface of osteoblasts and bone marrow stem cells. [1]

        Influenced by:

        • PTHR1
          in hematopoietic_stem_cell
        • VDR
          in hematopoietic_stem_cell
      • Hormone: interleukin 6

        • Sex hormones suppress the synthesis and secretion of IL-6 by osteoblasts and bone marrow stem cells. [1]
      • Hormone: FGF-2

      • Hormone: Granulin-1

        • PGRN is highly expressed by cells with a high mitotic rate and low expression is found in tissues with less proliferative activity. [2]


      • Receptor: VDR


        • RANKL
      • Receptor: PTHR1


        • RANKL
      • Receptor: GM-CSFR

        • The receptors for GM-CSF, IL-3, and IL-5 are expressed at very low levels (100–1000 per cell) on the surface of hematopoietic cells [3]

        Induced phenotype:

        • leukocyte production
      • Receptor: M-CSF-1-R

      • Receptor: SCFR

      • Receptor: IL -3R

      • Receptor: ALCAM

      • Receptor: FLT3

        • In human hematopoietic cells, FLT3 expression is restricted to the CD34-positive fraction of bone marrow and a smaller fraction of CD34-negative cells destined to become dendritic cells. [4]

        Induced phenotype:

        • hematopoiesis
          • The accumulated data clearly point to FLT3 as an important receptor in early hematopoiesis. [4]
        • Acute myeloid leukemia
          • Deregulated tyrosine kinase activity has long been implicated in the molecular pathogenesis of cancer, including leukemia, and mutant forms of KIT, ABL, and platelet-derived growth factor receptor (PDGF-R) number among the constitutively activated tyrosine kinases that have been identified as causative factors in specific hematologic malignancies. [4]
          • FMS-like tyrosine kinase-3 (FLT3), a member of the PDGF-R subfamily of receptor tyrosine kinases, is the most recent major addition to this list [4]
          • A number of FLT3 activating mutations have been found in leukemia patients and human leukemia-derived cell lines. [4]
          • FLT3 activating mutations occur in 30% of AML cases and are therefore the most common molecular abnormality in that disease. [4]