Suotian相关文献与解析，生知库 | 链接生命科学的每一步

Wang, Xu; Tan, Jinfeng; Tang, Jie; Wang, Teng; Zeng, Dachuan; Zheng, Renren; Hu, Jing; Liu, Suotian; Wei, Wei; Zou, Jie; Du, Yan; Huang, Zhenglan; Gao, Miao

白血病

PKC

发表日期：2025

文献求助收藏

The FABD domain is critical for the oncogenicity of BCR/ABL in chronic myeloid leukaemia

FABD结构域对于BCR/ABL在慢性粒细胞白血病中的致癌性至关重要。

期刊:Cell Communication and Signaling

影响因子:8.9

doi:10.1186/s12964-024-01694-8

Zheng, Renren; Wei, Wei; Liu, Suotian; Zeng, Dachuan; Yang, Zesong; Tang, Jie; Tan, Jinfeng; Huang, Zhenglan; Gao, Miao

mTOR inhibition by AZD2014 alleviates BCR::ABL1 independent imatinib resistance through enhancing autophagy in CML resistant cells

AZD2014 通过抑制 mTOR 增强 CML 耐药细胞中的自噬作用，从而缓解 BCR::ABL1 非依赖性伊马替尼耐药性。

期刊:American Journal of Cancer Research

影响因子:2.9

doi:10.62347/RWLJ3990

He, Wei; Liu, Suotian; Wei, Wei; Qin, Run; Tan, Jinfeng; Tang, Jie; Huang, Zhenglan; Gao, Miao

Jak2/STAT6/c-Myc pathway is vital to the pathogenicity of Philadelphia-positive acute lymphoblastic leukemia caused by P190(BCR-ABL)

Jak2/STAT6/c-Myc通路对于P190(BCR-ABL)引起的费城染色体阳性急性淋巴细胞白血病的致病性至关重要。

期刊:Cell Communication and Signaling

影响因子:8.9

doi:10.1186/s12964-023-01039-x

Qin, Run; Wang, Teng; He, Wei; Wei, Wei; Liu, Suotian; Gao, Miao; Huang, Zhenglan

The HSP90 inhibitor KW-2478 depletes the malignancy of BCR/ABL and overcomes the imatinib-resistance caused by BCR/ABL amplification

HSP90 抑制剂 KW-2478 可消除 BCR/ABL 的恶性程度，并克服由 BCR/ABL 扩增引起的伊马替尼耐药性

期刊:Experimental Hematology & Oncology

影响因子:9.4

doi:10.1186/s40164-022-00287-w

Dachuan Zeng #, Miao Gao #, Renren Zheng #, Run Qin, Wei He, Suotian Liu, Wei Wei, Zhenglan Huang

CILP2: From ECM Component to a Pleiotropic Modulator in Metabolic Dysfunction, Cancer, and Beyond

CILP2：从细胞外基质成分到代谢功能障碍、癌症及其他领域的多效性调节因子

PMA exerts anti-leukemia effect in Ph(+) ALL through activating PKC δ and its down-stream molecules

PMA通过激活PKCδ及其下游分子，在Ph(+) ALL中发挥抗白血病作用。

The FABD domain is critical for the oncogenicity of BCR/ABL in chronic myeloid leukaemia

FABD结构域对于BCR/ABL在慢性粒细胞白血病中的致癌性至关重要。

mTOR inhibition by AZD2014 alleviates BCR::ABL1 independent imatinib resistance through enhancing autophagy in CML resistant cells

AZD2014 通过抑制 mTOR 增强 CML 耐药细胞中的自噬作用，从而缓解 BCR::ABL1 非依赖性伊马替尼耐药性。

Jak2/STAT6/c-Myc pathway is vital to the pathogenicity of Philadelphia-positive acute lymphoblastic leukemia caused by P190(BCR-ABL)

Jak2/STAT6/c-Myc通路对于P190(BCR-ABL)引起的费城染色体阳性急性淋巴细胞白血病的致病性至关重要。

The HSP90 inhibitor KW-2478 depletes the malignancy of BCR/ABL and overcomes the imatinib-resistance caused by BCR/ABL amplification

HSP90 抑制剂 KW-2478 可消除 BCR/ABL 的恶性程度，并克服由 BCR/ABL 扩增引起的伊马替尼耐药性