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sirna against mouse ddit4 sc-142310 (Santa Cruz Biotechnology)

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Santa Cruz Biotechnology sirna against mouse ddit4 sc-142310
Sirna Against Mouse Ddit4 Sc 142310, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+ddit4/pmc11939615-95-0-11?v=Santa+Cruz+Biotechnology
Average 90 stars, based on 1 article reviews

sirna against mouse ddit4 sc-142310 - by Bioz Stars, 2026-07

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Figure 4. ATF4-induced DDIT4 and subsequent mTORC1 inhibition trigger ferroptotic signaling. (A) Western blot analysis of indicated proteins in AML12 cells after Torin1 treatment (0, 0.5, 1, and 2 µM) for 24 h. (B–D) AML12 cells were treated with erastin (5 µM) or Torin1 (0.5 µM) in the presence or absence of Fer-1 (10 µM) for 16 h. (B) Lipid ROS was stained with BODIPY™581/591 C11 and measured by flow cytometry. (C) Cell viability assessed by MTT. (D) Quantification of mRNA level of Ptgs2. (E) Western blot analysis of indicated proteins in AML12 after treatment with erastin (10 µM) at indicated times. (F–I) For knockdown Ddit4, AML12 cells were transfected with control siRNA (scRNA) or siDdit4 for 36 h. (F) Western blot analysis of indicated proteins after erastin (10 µM) treatment for 24 h. (G) Quantification of mRNA level of indicated genes. (H) Lipid ROS was stained with BODIPY™581/591 C11 and measured by flow cytometry. (I) Cell viability assessed by MTT assay after erastin treatment (0, 1.25, 2.5, 5, 10, and 20 µM) for 24 h. (J) Atf4−/−cells were infected with Ad-GFP or Ad-ATF4 and then treated with erastin (10 µM) for 24 h. Western blot analysis of indicated proteins. (K–L) Ad-GFP and Ad-ATF4 were infected in scRNA or siDdit4-transfected AML12 cells followed by erastin (10 µM) treatment for 24 h. (K) Western blot analysis of indicated proteins. (L) Lipid ROS was stained with BODIPY™581/591 C11 and measured by flow cytometry. Data are mean ± SD (n = 3); * p < 0.05, ** p < 0.01, *** p < 0.001, and NS, not significant.

Journal: Antioxidants (Basel, Switzerland)

Article Title: The PERK-eIF2α-ATF4 Axis Is Involved in Mediating ER-Stress-Induced Ferroptosis via DDIT4-mTORC1 Inhibition and Acetaminophen-Induced Hepatotoxicity.

doi: 10.3390/antiox14030307

Figure Lengend Snippet: Figure 4. ATF4-induced DDIT4 and subsequent mTORC1 inhibition trigger ferroptotic signaling. (A) Western blot analysis of indicated proteins in AML12 cells after Torin1 treatment (0, 0.5, 1, and 2 µM) for 24 h. (B–D) AML12 cells were treated with erastin (5 µM) or Torin1 (0.5 µM) in the presence or absence of Fer-1 (10 µM) for 16 h. (B) Lipid ROS was stained with BODIPY™581/591 C11 and measured by flow cytometry. (C) Cell viability assessed by MTT. (D) Quantification of mRNA level of Ptgs2. (E) Western blot analysis of indicated proteins in AML12 after treatment with erastin (10 µM) at indicated times. (F–I) For knockdown Ddit4, AML12 cells were transfected with control siRNA (scRNA) or siDdit4 for 36 h. (F) Western blot analysis of indicated proteins after erastin (10 µM) treatment for 24 h. (G) Quantification of mRNA level of indicated genes. (H) Lipid ROS was stained with BODIPY™581/591 C11 and measured by flow cytometry. (I) Cell viability assessed by MTT assay after erastin treatment (0, 1.25, 2.5, 5, 10, and 20 µM) for 24 h. (J) Atf4−/−cells were infected with Ad-GFP or Ad-ATF4 and then treated with erastin (10 µM) for 24 h. Western blot analysis of indicated proteins. (K–L) Ad-GFP and Ad-ATF4 were infected in scRNA or siDdit4-transfected AML12 cells followed by erastin (10 µM) treatment for 24 h. (K) Western blot analysis of indicated proteins. (L) Lipid ROS was stained with BODIPY™581/591 C11 and measured by flow cytometry. Data are mean ± SD (n = 3); * p < 0.05, ** p < 0.01, *** p < 0.001, and NS, not significant.

Article Snippet: Small Interfering RNA Transfection Small interfering RNA (siRNA) against mouse Ddit4 (siDdit4) (sc-142310, Santa Cruz, Dallas, TX, USA) was purchased from Santa Cruz Biotechnology, and negative control siRNA (scRNA) (AM4611, Ambion, Austin, TX, USA) was purchased from Ambion.

Techniques: Inhibition, Western Blot, Staining, Flow Cytometry, Knockdown, Transfection, Control, MTT Assay, Infection

List of primers for qRT-PCR analysis of gene expression. F—forward, R—reverse, bs—bases.

Journal: Antioxidants

Article Title: The PERK-eIF2α-ATF4 Axis Is Involved in Mediating ER-Stress-Induced Ferroptosis via DDIT4-mTORC1 Inhibition and Acetaminophen-Induced Hepatotoxicity

doi: 10.3390/antiox14030307

Figure Lengend Snippet: List of primers for qRT-PCR analysis of gene expression. F—forward, R—reverse, bs—bases.

Article Snippet: Small interfering RNA (siRNA) against mouse Ddit4 ( siDdit4 ) (sc-142310, Santa Cruz, Dallas, TX, USA) was purchased from Santa Cruz Biotechnology, and negative control siRNA ( scRNA ) (AM4611, Ambion, Austin, TX, USA) was purchased from Ambion.

Techniques: Gene Expression, Sequencing

ATF4-induced DDIT4 and subsequent mTORC1 inhibition trigger ferroptotic signaling. ( A ) Western blot analysis of indicated proteins in AML12 cells after Torin1 treatment (0, 0.5, 1, and 2 μM) for 24 h. ( B – D ) AML12 cells were treated with erastin (5 μM) or Torin1 (0.5 μM) in the presence or absence of Fer-1 (10 μM) for 16 h. ( B ) Lipid ROS was stained with BODIPY™ 581/591 C11 and measured by flow cytometry. ( C ) Cell viability assessed by MTT. ( D ) Quantification of mRNA level of Ptgs2 . ( E ) Western blot analysis of indicated proteins in AML12 after treatment with erastin (10 μM) at indicated times. ( F – I ) For knockdown Ddit4 , AML12 cells were transfected with control siRNA ( scRNA ) or siDdit4 for 36 h. ( F ) Western blot analysis of indicated proteins after erastin (10 μM) treatment for 24 h. ( G ) Quantification of mRNA level of indicated genes. ( H ) Lipid ROS was stained with BODIPY™ 581/591 C11 and measured by flow cytometry. ( I ) Cell viability assessed by MTT assay after erastin treatment (0, 1.25, 2.5, 5, 10, and 20 μM) for 24 h. ( J ) Atf4 −/− cells were infected with Ad-GFP or Ad-ATF4 and then treated with erastin (10 μM) for 24 h. Western blot analysis of indicated proteins. ( K – L ) Ad-GFP and Ad-ATF4 were infected in scRNA or siDdit4 -transfected AML12 cells followed by erastin (10 μM) treatment for 24 h. ( K ) Western blot analysis of indicated proteins. ( L ) Lipid ROS was stained with BODIPY™ 581/591 C11 and measured by flow cytometry. Data are mean ± SD ( n = 3); * p < 0.05, ** p < 0.01, *** p < 0.001, and NS, not significant.

Journal: Antioxidants

Article Title: The PERK-eIF2α-ATF4 Axis Is Involved in Mediating ER-Stress-Induced Ferroptosis via DDIT4-mTORC1 Inhibition and Acetaminophen-Induced Hepatotoxicity

doi: 10.3390/antiox14030307

Figure Lengend Snippet: ATF4-induced DDIT4 and subsequent mTORC1 inhibition trigger ferroptotic signaling. ( A ) Western blot analysis of indicated proteins in AML12 cells after Torin1 treatment (0, 0.5, 1, and 2 μM) for 24 h. ( B – D ) AML12 cells were treated with erastin (5 μM) or Torin1 (0.5 μM) in the presence or absence of Fer-1 (10 μM) for 16 h. ( B ) Lipid ROS was stained with BODIPY™ 581/591 C11 and measured by flow cytometry. ( C ) Cell viability assessed by MTT. ( D ) Quantification of mRNA level of Ptgs2 . ( E ) Western blot analysis of indicated proteins in AML12 after treatment with erastin (10 μM) at indicated times. ( F – I ) For knockdown Ddit4 , AML12 cells were transfected with control siRNA ( scRNA ) or siDdit4 for 36 h. ( F ) Western blot analysis of indicated proteins after erastin (10 μM) treatment for 24 h. ( G ) Quantification of mRNA level of indicated genes. ( H ) Lipid ROS was stained with BODIPY™ 581/591 C11 and measured by flow cytometry. ( I ) Cell viability assessed by MTT assay after erastin treatment (0, 1.25, 2.5, 5, 10, and 20 μM) for 24 h. ( J ) Atf4 −/− cells were infected with Ad-GFP or Ad-ATF4 and then treated with erastin (10 μM) for 24 h. Western blot analysis of indicated proteins. ( K – L ) Ad-GFP and Ad-ATF4 were infected in scRNA or siDdit4 -transfected AML12 cells followed by erastin (10 μM) treatment for 24 h. ( K ) Western blot analysis of indicated proteins. ( L ) Lipid ROS was stained with BODIPY™ 581/591 C11 and measured by flow cytometry. Data are mean ± SD ( n = 3); * p < 0.05, ** p < 0.01, *** p < 0.001, and NS, not significant.

Techniques: Inhibition, Western Blot, Staining, Flow Cytometry, Knockdown, Transfection, Control, MTT Assay, Infection

Fig. 2. DINP upregulates DDIT4 expression in ovarian granulosa cells. (A) DDIT4 expression in the ovary tissue was detected by IHC after adult female mice were administered with 0–200 mg/kg DINP for 14 days. The scale bar was 100 µm. (B) The mRNA level of DDIT4 was determined by qPCR after KGN cells were exposed to 0 or 800 μM DINP for 24 h. (C, D) The protein expression of DDIT4 was detected by Western blot after KGN cells were exposed to 0–800 μM DINP for 24 h. *P < 0.05.

Journal: Ecotoxicology and environmental safety

Article Title: DDIT4 is essential for DINP-induced autophagy of ovarian granulosa cells.

doi: 10.1016/j.ecoenv.2023.115686

Figure Lengend Snippet: Fig. 2. DINP upregulates DDIT4 expression in ovarian granulosa cells. (A) DDIT4 expression in the ovary tissue was detected by IHC after adult female mice were administered with 0–200 mg/kg DINP for 14 days. The scale bar was 100 µm. (B) The mRNA level of DDIT4 was determined by qPCR after KGN cells were exposed to 0 or 800 μM DINP for 24 h. (C, D) The protein expression of DDIT4 was detected by Western blot after KGN cells were exposed to 0–800 μM DINP for 24 h. *P < 0.05.

Article Snippet: Rabbit anti-DDIT4 polyclonal antibody (10638–1-AP) and mouse IgG (B900620) were purchased from Proteintech Group, Inc (Wuhan, China).

Techniques: Expressing, Western Blot

Fig. 3. DDIT4 is essential for DINP-induced autophagy of ovarian granulosa cells. (A, B) The protein levels of LC3, Beclin 1, Atg 5, p62 and DDIT4 were determined by Western blot after KGN cells were transfected with 0, 1, 2 μg pcDNA3.1-DDIT4 plasmid for 48 h. (C) Autophagic vesicles were observed by TEM after KGN cells were transfected with 0 or 2 μg pcDNA3.1-DDIT4 for 48 h. (D, E) The expression of LC3, Beclin 1, Atg 5, p62 and DDIT4 in KGN cells was detected by Western blot after the cells were transfected with si-NC or si-DDIT4 for 24 h. The protein levels of LC3, Beclin 1, Atg 5, p62 and DDIT4 (F, G) and the DDIT4 mRNA level (H) in KGN cells were detected after the cells were exposed to 0 or 800 μM DINP in the presence or absence of si-DDIT4 for 24 h.*P < 0.05.

Journal: Ecotoxicology and environmental safety

Article Title: DDIT4 is essential for DINP-induced autophagy of ovarian granulosa cells.

doi: 10.1016/j.ecoenv.2023.115686

Figure Lengend Snippet: Fig. 3. DDIT4 is essential for DINP-induced autophagy of ovarian granulosa cells. (A, B) The protein levels of LC3, Beclin 1, Atg 5, p62 and DDIT4 were determined by Western blot after KGN cells were transfected with 0, 1, 2 μg pcDNA3.1-DDIT4 plasmid for 48 h. (C) Autophagic vesicles were observed by TEM after KGN cells were transfected with 0 or 2 μg pcDNA3.1-DDIT4 for 48 h. (D, E) The expression of LC3, Beclin 1, Atg 5, p62 and DDIT4 in KGN cells was detected by Western blot after the cells were transfected with si-NC or si-DDIT4 for 24 h. The protein levels of LC3, Beclin 1, Atg 5, p62 and DDIT4 (F, G) and the DDIT4 mRNA level (H) in KGN cells were detected after the cells were exposed to 0 or 800 μM DINP in the presence or absence of si-DDIT4 for 24 h.*P < 0.05.

Article Snippet: Rabbit anti-DDIT4 polyclonal antibody (10638–1-AP) and mouse IgG (B900620) were purchased from Proteintech Group, Inc (Wuhan, China).

Techniques: Western Blot, Transfection, Plasmid Preparation, Expressing

Fig. 4. ATF4 promotes gene transcription of DDIT4. (A) Three potential ATF4 responsive elements (RE) in the DDIT4 promoter region were predicted by JASPAR. (B- D) The mRNA and protein levels of ATF4 and DDIT4 were detected by qPCR and Western blot, respectively, after KGN cells were transfected with 0, 1, 2 μg pcDNA3.1-ATF4 for 24 or 48 h. (E-G) The mRNA and protein levels of ATF4 and DDIT4 were determined by qPCR and Western blot, respectively, after KGN cells were transfected with si-NC or si-ATF4 for 24 h. (H) Luciferase activity was detected after KGN cells were transfected with pGL4.2 or pGL4.2-DDIT4 prom together with pcDNA3.1 or pcDNA3.1-ATF4 for 48 h. (I) Luciferase activity was determined after KGN cells were transfected with pGL4.2-RE1, pGL4.2-RE2 or pGL4.2-RE3, respectively, together with pcDNA3.1 or pcDNA3.1-ATF4 for 48 h. (J) Luciferase activity was determined after KGN cells were transfected with pGL4.2-RE2 or pGL4.2-mutRE2 for 48 h in the presence or absence of pcDNA3.1-ATF4. (K) ChIP-qPCR analysis was utilized to identify the binding of ATF4 to the RE2 site. *P < 0.05.

Journal: Ecotoxicology and environmental safety

Article Title: DDIT4 is essential for DINP-induced autophagy of ovarian granulosa cells.

doi: 10.1016/j.ecoenv.2023.115686

Figure Lengend Snippet: Fig. 4. ATF4 promotes gene transcription of DDIT4. (A) Three potential ATF4 responsive elements (RE) in the DDIT4 promoter region were predicted by JASPAR. (B- D) The mRNA and protein levels of ATF4 and DDIT4 were detected by qPCR and Western blot, respectively, after KGN cells were transfected with 0, 1, 2 μg pcDNA3.1-ATF4 for 24 or 48 h. (E-G) The mRNA and protein levels of ATF4 and DDIT4 were determined by qPCR and Western blot, respectively, after KGN cells were transfected with si-NC or si-ATF4 for 24 h. (H) Luciferase activity was detected after KGN cells were transfected with pGL4.2 or pGL4.2-DDIT4 prom together with pcDNA3.1 or pcDNA3.1-ATF4 for 48 h. (I) Luciferase activity was determined after KGN cells were transfected with pGL4.2-RE1, pGL4.2-RE2 or pGL4.2-RE3, respectively, together with pcDNA3.1 or pcDNA3.1-ATF4 for 48 h. (J) Luciferase activity was determined after KGN cells were transfected with pGL4.2-RE2 or pGL4.2-mutRE2 for 48 h in the presence or absence of pcDNA3.1-ATF4. (K) ChIP-qPCR analysis was utilized to identify the binding of ATF4 to the RE2 site. *P < 0.05.

Article Snippet: Rabbit anti-DDIT4 polyclonal antibody (10638–1-AP) and mouse IgG (B900620) were purchased from Proteintech Group, Inc (Wuhan, China).

Techniques: Western Blot, Transfection, Luciferase, Activity Assay, ChIP-qPCR, Binding Assay

Fig. 5. ATF4 is involved in DINP-induced upregulation of DDIT4 in ovarian granulosa cells. (A) The ATF4 expression in the ovary tissue was observed by IHC after adult female mice were administered with 0–200 mg/kg DINP for 14 d. The scale bar was 20 µm. (B-D) The ATF4 mRNA and protein level were detected by qPCR and Western blot, respectively, after KGN cells were treated with the indicated concentration of DINP for 24 h. (E-G) The expression of DDIT4 and ATF4 was detected by qPCR and Western blot, respectively, after KGN cells were exposed to 0 or 800 μM DINP for 24 h in the presence or absence of si-ATF4. *P < 0.05.

Journal: Ecotoxicology and environmental safety

Article Title: DDIT4 is essential for DINP-induced autophagy of ovarian granulosa cells.

doi: 10.1016/j.ecoenv.2023.115686

Figure Lengend Snippet: Fig. 5. ATF4 is involved in DINP-induced upregulation of DDIT4 in ovarian granulosa cells. (A) The ATF4 expression in the ovary tissue was observed by IHC after adult female mice were administered with 0–200 mg/kg DINP for 14 d. The scale bar was 20 µm. (B-D) The ATF4 mRNA and protein level were detected by qPCR and Western blot, respectively, after KGN cells were treated with the indicated concentration of DINP for 24 h. (E-G) The expression of DDIT4 and ATF4 was detected by qPCR and Western blot, respectively, after KGN cells were exposed to 0 or 800 μM DINP for 24 h in the presence or absence of si-ATF4. *P < 0.05.

Article Snippet: Rabbit anti-DDIT4 polyclonal antibody (10638–1-AP) and mouse IgG (B900620) were purchased from Proteintech Group, Inc (Wuhan, China).

Techniques: Expressing, Western Blot, Concentration Assay

Fig. 6. DINP induces autophagy of ovarian granulosa cells via ATF4/DDIT4 signals. (A, B) The protein levels of LC3, Atg 5, Beclin 1, p62 and ATF4 were determined after KGN cells were transfected with 0, 1, 2 μg pcDNA3.1-ATF4 for 48 h. (C) Autophagic vesicles were detected by TEM after KGN cells were transfected with 0 or 2 μg pcDNA3.1-ATF4 for 48 h. (D, E) The protein levels of LC3, Beclin 1, Atg 5, p62 and ATF4 were detected after KGN cells were transfected with si-NC or si-ATF4 for 24 h. (F, G) The protein levels of LC3, Beclin 1, Atg 5, p62 and ATF4 were determined after KGN cells were exposed to 0 or 800 μM DINP for 24 h in the presence or absence of si-ATF. *P < 0.05.

Journal: Ecotoxicology and environmental safety

Article Title: DDIT4 is essential for DINP-induced autophagy of ovarian granulosa cells.

doi: 10.1016/j.ecoenv.2023.115686

Figure Lengend Snippet: Fig. 6. DINP induces autophagy of ovarian granulosa cells via ATF4/DDIT4 signals. (A, B) The protein levels of LC3, Atg 5, Beclin 1, p62 and ATF4 were determined after KGN cells were transfected with 0, 1, 2 μg pcDNA3.1-ATF4 for 48 h. (C) Autophagic vesicles were detected by TEM after KGN cells were transfected with 0 or 2 μg pcDNA3.1-ATF4 for 48 h. (D, E) The protein levels of LC3, Beclin 1, Atg 5, p62 and ATF4 were detected after KGN cells were transfected with si-NC or si-ATF4 for 24 h. (F, G) The protein levels of LC3, Beclin 1, Atg 5, p62 and ATF4 were determined after KGN cells were exposed to 0 or 800 μM DINP for 24 h in the presence or absence of si-ATF. *P < 0.05.

Article Snippet: Rabbit anti-DDIT4 polyclonal antibody (10638–1-AP) and mouse IgG (B900620) were purchased from Proteintech Group, Inc (Wuhan, China).

Techniques: Transfection

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