2. GPCR/G Protein MAPK/ERK Pathway Apoptosis Stem Cell/Wnt Cell Cycle/DNA Damage
  3. Ras Apoptosis MEK ERK CDK
  4. GIT1-IN-1

GIT1-IN-1 是一种 ARF GTP 酶蛋白 1 (GIT1) 抑制剂，其 KD 为 6.2 μM。GIT1-IN-1 可诱导肝癌和结肠癌细胞凋亡 (apoptosis)，阻滞 G2/M 细胞周期，抑制细胞增殖、集落形成及迁移。GIT1-IN-1 可抑制肝癌和结肠癌细胞中 MEK 与 ERK 的活性，降低 cyclin D1 的表达水平，稳定 cyclin B1 蛋白。GIT1-IN-1 可用于肝癌、结肠癌的研究。

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GIT1-IN-1

GIT1-IN-1 Chemical Structure

CAS No. : 844464-54-6

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GIT1-IN-1 相关抗体

Top Publications Citing Use of Products

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K-Ras H-Ras N-Ras Ras

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MEK1 MEK2 MEK5 MEK MAP2K4/MEK4

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ERK ERK1 ERK2 ERK5 ERK8

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CDK1 CDK2 CDK3 CDK4 CDK5 CDK6 CDK7 CDK8 CDK9 CDK11 CDK12 CDK13 CDK14 CDK16 CDK19 CDC CLK Pho85 CDK10 CDK15 CDK17 CDK18 CDK20 PITSLRE

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

GIT1-IN-1 is an inhibitor of ARF GTPase-activating protein 1 (GIT1) with a KD of 6.2 μM. GIT1-IN-1 induces apoptosis (apoptosis) in liver and colon cancer cells, arrests the cell cycle at the G2/M phase, and inhibits cell proliferation, colony formation and migration. GIT1-IN-1 inhibits the activities of MEK and ERK, reduces the expression level of cyclin D1, and stabilizes cyclin B1 protein in liver and colon cancer cells. GIT1-IN-1 can be used in the research of liver cancer and colon cancer[1].

IC50 & Target[1]

ERK1

 

ERK2

 

MEK1

 

MEK2

 

CDK1/cyclinB1

 

体外研究
(In Vitro)

GIT1-IN-1 (Compound C3) (10-100 μM; 24 h) 可抑制 HepG2、Hep3B、MzChA-1、HT-29 及 RKO 肝癌和结肠癌细胞的活力与增殖，其 IC50 约为 20 μM，但在最高 100 μM 的浓度下对非恶性的 AML12、HEK293 细胞或原代小鼠及人肝细胞无影响[1]。
GIT1-IN-1 (1-5 μM; 24 h) 可在 HepG2 和 RKO 肝癌及结肠癌细胞中诱导剂量依赖性 G2/M 期阻滞，但对非恶性 AML12 或 HEK293 细胞的细胞周期进程无影响[1]。
GIT1-IN-1 (5 μM; 24-48 h) 可在 RKO 结肠癌细胞中诱导时间依赖性细胞凋亡，且在 48 小时后增加 HepG2 肝癌细胞的凋亡与坏死，但不会在非恶性的 AML12 细胞、HEK293 细胞或原代小鼠/人肝细胞中诱导细胞死亡[1]。
GIT1-IN-1 (1-10 μM; 24 h) 以剂量依赖的方式抑制 HepG2 肝癌细胞和 RKO 结肠癌细胞的克隆形成，但不影响非恶性 AML12 细胞[1]。
GIT1-IN-1 (1-2 μM; 24 h) 可呈剂量依赖性抑制 RKO 结肠癌细胞和 MzChA-1 肝癌细胞的迁移[1]。
GIT1-IN-1 (5-10 μM; 24 h) 在 10 μM 浓度下可破坏 HepG2 和 RKO 肝癌及结肠癌细胞中 GIT1-MAT2B 与 MEK1/2-cRAF/BRAF/ERK1/2/GIT1 的相互作用；在 5 μM 浓度下可破坏该细胞中 GIT1-CDC20、GIT1-APC3、cyclin B1-CDC20 及 cyclin B1-APC3 的相互作用，同时增强 GIT1-cyclin B1 的相互作用[1]。
GIT1-IN-1 (2-10 μM; 24 h) 可抑制 HepG2、RKO 和 MC38 肝癌及结肠癌细胞中 MEK 与 ERK 通路的活性，表现为 pMEK1/2、pERK1/2 和细胞周期蛋白 D1 水平降低，但对非恶性 AML12 细胞中的该通路活性无影响[1]。
GIT1-IN-1 (2-5 μM; 24 h) 可在 HepG2 和 RKO 肝癌及结肠癌细胞中提升 cyclin B1 蛋白稳定性、促进 cyclin B1-CDK1 复合物形成并增强 CDK1 活性，这一点可通过 cyclin B1 半衰期延长、CDK1 抑制性磷酸化水平降低以及 cyclin B1 激活型磷酸化水平升高得到证明[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

GIT1-IN-1 相关抗体:

Cell Viability Assay[1]

Cell Line: HepG2, Hep3B, MzChA-1, HT-29, RKO, AML12, HEK293, primary mouse hepatocytes, primary human hepatocytes
Concentration: 10 μM; 50 μM; 100 μM
Incubation Time: 24 h
Result: Inhibited growth of HepG2, Hep3B, MzChA-1, HT-29, and RKO cells at 10 μM.
Exhibited dose-dependent reduction in viability and proliferation of cancer cells at 10, 50, and 100 μM.
Exerted dose-dependent inhibition of cancer cell viability with an IC50 of around 20 μM.
Did not reduce viability or proliferation in AML12, HEK293, primary mouse hepatocytes, or primary human hepatocytes at concentrations up to 100 μM.

Cell Cycle Analysis[1]

Cell Line: HepG2, RKO, AML12, HEK293
Concentration: 1 μM; 2 μM; 5 μM
Incubation Time: 24 h
Result: Reduced the percentage of HepG2 and RKO cells in the G1 phase.
Significantly increased the percentage of HepG2 and RKO cells in the G2/M phase, indicating G2/M phase arrest.
Induced dose-dependent G2/M phase arrest in HepG2 and RKO cells at concentrations from 1 to 5 μM.
Caused no G2/M arrest in AML12 or HEK293 cells.

Apoptosis Analysis[1]

Cell Line: HepG2, RKO, AML12, HEK293, primary mouse hepatocytes, primary human hepatocytes
Concentration: 5 μM
Incubation Time: 24 h; 48 h
Result: Induced significant time-dependent apoptosis in RKO cells.
Increased apoptosis and necrosis significantly in HepG2 cells after 48 hours of treatment, though absolute values remained low.
Caused no increase in apoptosis or necrosis in AML12, HEK293, primary mouse hepatocytes, or primary human hepatocytes after 48 hours of treatment.

Cell Migration Assay[1]

Cell Line: RKO, MzChA-1
Concentration: 1 μM; 2 μM
Incubation Time: 24 h
Result: Induced dose-dependent inhibition of cell migration in both RKO and MzChA-1 cells at 1 and 2 μM, measured as reduced scratch closure relative to baseline.

Western Blot Analysis[1]

Cell Line: HepG2, RKO
Concentration: 5 μM; 10 μM
Incubation Time: 24 h
Result: Reduced the interaction between GIT1 and MAT2B in HepG2 cells at 10 μM.
Reduced recruitment of cRAF, BRAF, ERK1/2, and GIT1 to MEK1/2 in HepG2 and RKO cells at 10 μM.
Reduced interactions between GIT1 and CDC20, GIT1 and APC3, cyclin B1 and CDC20, and cyclin B1 and APC3 in HepG2 and RKO cells at 5 μM.
Enhanced the interaction between GIT1 and cyclin B1 in HepG2 cells at 5 μM.

Western Blot Analysis[1]

Cell Line: HepG2, RKO, MC38, AML12
Concentration: 2 μM; 3 μM; 5 μM; 10 μM
Incubation Time: 24 h
Result: Reduced phosphorylated MEK1/2 (pMEK1/2) levels in HepG2 and RKO cells at 2, 3, and 5 μM.
Reduced phosphorylated ERK1/2 (pERK1/2) and cyclin D1 levels in HepG2 and MC38 cells at 10 μM.
Caused no effect on pMEK1/2, pERK1/2, or cyclin D1 levels in AML12 cells.

Western Blot Analysis[1]

Cell Line: HepG2, RKO, MC38
Concentration: 2 μM; 3 μM; 5 μM
Incubation Time: 24 h; 0, 1, 2, 4, 6 h (with CHX pretreatment)
Result: Caused dose-dependent increase in cyclin B1 protein levels in HepG2 cells at 2, 3, and 5 μM.
Induced slight increase in cyclin B1 mRNA level (≤ 30%) and significant stabilization of cyclin B1 protein in HepG2 cells, prolonging the half-life of cyclin B1 from 3.6 h to > 24 h.
Increased formation of the cyclin B1-CDK1 complex in HepG2 and RKO cells.
Reduced inhibitory phosphorylation of CDK1 (p-Thr14/p-Tyr15) in HepG2 and MC38 cells.
Increased activating phosphorylation of cyclin B1 (p-S116) in HepG2 cells.
体内研究
(In Vivo)

GIT1-IN-1 (Compound C3) (100 μM；瘤内注射；每 2 天 1 次；共 6 天) 在 C57BL/6 小鼠中可通过抑制 MEK 活性显著抑制结直肠癌皮下移植瘤生长、降低肿瘤细胞增殖并促进细胞凋亡[1]。
GIT1-IN-1 (25 mg/kg；腹腔注射；每日 1 次；连续 5 天) 可显著抑制裸鼠体内人结直肠癌肝内异种移植物的生长[1]。
GIT1-IN-1 (15-20 mg/kg；腹腔注射；间歇性给药) 可显著抑制免疫健全的 C57BL/6 小鼠的结直肠癌肝转移，且不会产生可检测到的肝毒性[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6 (both sexes)[1]
Dosage: 100 μM
Administration: intratumoral; every other day; 6 days
Result: Reduced tumor volume significantly compared to DMSO control.
Increased apoptotic cells significantly (TUNEL staining).
Reduced proliferation score significantly (PCNA staining).
Decreased phosphorylated MEK1/2 (Ser218/222) activity significantly relative to total MEK1/2, while GIT1 protein levels remained unchanged.
Changed MC38 tumor cells from spindle-shaped to small round cells (histological analysis).
Animal Model: Nude (male, 4 months old)[1]
Dosage: 25 mg/kg
Administration: intraperitoneal; daily; 5 days
Result: Reduced liver tumor bioluminescent intensity significantly relative to baseline and DMSO control.
Reduced tumor burden compared to DMSO-treated mice (gross liver examination).
Animal Model: C57BL/6 (both sexes)[1]
Dosage: 20 mg/kg (day 1); 15 mg/kg (daily for 3 days, then daily for 2 days after 2-day rest)
Administration: intraperitoneal; intermittent dosing (20 mg/kg day 1, then 15 mg/kg daily ×3, 2-day rest, 15 mg/kg daily ×2)
Result: Reduced bioluminescent intensity significantly relative to DMSO control, indicating inhibited liver tumor growth and metastasis.
Showed no significant difference in plasma ALT and AST levels compared to DMSO control, indicating no overt hepatic toxicity.
Reduced tumor burden compared to DMSO-treated mice (histological analysis).
分子量

424.47

Formula

C21H20N4O4S
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

GIT1-IN-1 相关分类

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  • Do most proteins show cross-species activity?

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Keywords:

GIT1-IN-1844464-54-6RasApoptosisMEKERKCDKMitogen-activated protein kinase kinaseMAPKKMAP2KExtracellular signal regulated kinasesCyclin dependent kinaseankyrin repeat domainMEK1/2MAT2BGIT1cRAFBRAFliver cancer cellscolon cancer cellscyclin B1ERK1/2Inhibitorinhibitorinhibit

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