CSF3R (Colony stimulating factor 3 receptor)编码细胞因子-结肠刺激因子3的跨膜受体，也被称为G-CSF（粒细胞集落刺激因子）受体。受体的激活与嗜中性粒细胞的增加有关，临床上用于缩短化疗的恢复时间，并使造血干细胞流动进入外周血以收集干细胞。来自该受体的信号是由JAK（Janus激酶）和SRC（SRC 原癌基因）家族的激酶介导，并伴有对下游STAT,PI3K和MAPK信号级联的激活，以及通过SOCS（细胞因子信号转导抑制蛋白）蛋白和酪氨酸磷酸酶介导的抑制。CSF3R功能缺失突变可能导致严重的先天性中性粒细胞减少症。 CSF3R激活突变可以引起受体二聚化，而不依赖于具有近膜区域附近突变的配体或截短受体导致信号转导改变。在慢性粒细胞白血病、非典型慢性粒细胞白血病和急性髓性白血病等髓系疾病中检测到CSF3R的突变。在实体瘤中已被证明CSF3R表达对于疾病表型或转化起到重要作用。

CSF3R (Colony stimulating factor 3 receptor) encodes for a transmembrane receptor for cytokine colon stimulating factor 3; it also known as the G-CSF (Granulocyte-colony stimulating factor) receptor. Activation of the receptor is associated with the increased production of neutrophilic granulocytes and has been used clinically to shorten recovery time for chemotherapy and to mobilize hematopoietic stem cells into the periphery for stem cell collection. Signaling from the receptor is mediated by JAK (Janus kinase) and SRC (SRC proto-oncogene) family of kinases with downstream activation of STAT, PI3K, and MAPK signaling cascades and inhibition mediated through the SOCS (Suppressor of Cytokine Signaling) proteins and tyrosine phosphatases. Loss of function mutations can lead to severe congenital neutropenia. Activating mutations can cause receptor dimerization independent of ligand with mutations near the juxtamembrane region or truncate the receptor leading to altered signal transduction. These mutations have been found in myeloid disorders such as chronic neutrophilic leukemia, atypical chronic myeloid leukemia, and acute myeloid leukemia. Solid tumors have been shown to express CSF3R that may be important for disease phenotype or transformation.

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