Journal: Cell Stress & Chaperones

Article Title: Activation of unfolded protein response pathways promotes keratinocyte differentiation and ameliorates psoriasis phenotypes

doi: 10.1016/j.cstres.2026.100163

Figure Lengend Snippet: ER stress activity is decreased in IMQ-induced psoriatic mice. (a) Representative IHC images of untreated mouse skin and IMQ-induced psoriatic lesions stained for Grp78, XBP1s, and PERK. Expression of ER stress markers was significantly reduced in IMQ-induced psoriasis ( N = 6) versus untreated control group ( N = 6). (b) Correlation analysis between Grp78 and IVL or KRT1 in IMQ-induced psoriatic mice ( N = 6) and untreated mouse skin samples ( N = 6). (c) Reduced ER stress activity correlated with altered keratinocyte differentiation and proliferation in psoriasis. Western blot analysis of IVL, KRT1, Grp78, p-PERK, XBP1s, and ATF6 in tissues from IMQ-induced psoriatic ( N = 8) and control mice ( N = 5). Scale bar=100 µm. ns: not significant, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: The following primary antibodies were used for immunoblotting: Grp78 (Santa Cruz, SC-13968), KRT1 (Abclonal, A9776), IVL (Abclonal, A8026), Ki67 (Abcam, ab16667), XBP1s (Abclonal, A17007), XBP1u (Proteintech, 25997-1-AP), PERK (Proteintech, 24390-1-AP), p-PERK (Abclonal, AP1501), ATF6 (Proteintech, 24169-1-AP), β-Actin (Santa Cruz, sc-47778).

Techniques: Activity Assay, Staining, Expressing, Control, Western Blot

Journal: Cell Stress & Chaperones

Article Title: Activation of unfolded protein response pathways promotes keratinocyte differentiation and ameliorates psoriasis phenotypes

doi: 10.1016/j.cstres.2026.100163

Figure Lengend Snippet: ER stress inducers attenuate psoriatic phenotypes via UPR pathways activation. (a) Representative IHC staining for XBP1s and PERK in lesion tissues from IMQ-induced mice with or without ER stress inducer TM/BFA treatment, with corresponding IHC scores. Scale bar=100 µm. (b) Time-course Western blot analysis of IVL, KRT1, Grp78, p-PERK/PERK, XBP1s/XBP1, and ATF6 in primary mouse keratinocytes (mKCs) treated with TM (0.1 μg/mL) or BFA (20 nM) for 0-48 h. Data are mean ± SEM. ns: not significant, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: The following primary antibodies were used for immunoblotting: Grp78 (Santa Cruz, SC-13968), KRT1 (Abclonal, A9776), IVL (Abclonal, A8026), Ki67 (Abcam, ab16667), XBP1s (Abclonal, A17007), XBP1u (Proteintech, 25997-1-AP), PERK (Proteintech, 24390-1-AP), p-PERK (Abclonal, AP1501), ATF6 (Proteintech, 24169-1-AP), β-Actin (Santa Cruz, sc-47778).

Techniques: Activation Assay, Immunohistochemistry, Western Blot

Journal: Cell Stress & Chaperones

Article Title: Activation of unfolded protein response pathways promotes keratinocyte differentiation and ameliorates psoriasis phenotypes

doi: 10.1016/j.cstres.2026.100163

Figure Lengend Snippet: Grp78 synergizes with ER stress inducers to promote keratinocyte differentiation. (a) and (b) Primary mouse keratinocytes were transfected with shRNA against GRP78 (shGrp78-mKCs) or non-targeting control (shnon-mKCs) and treated with TM (0.1 μg/mL) or BFA (20 nM) for 24 and 48 h. Expression of IVL and KRT1, Grp78, p-PERK/PERK, XBP1s/XBP1, and ATF6 was assessed by Western blot. (c) and (d) HaCaT cells expressing shGrp78 (shGrp78-HaCaT) or control shRNA (shnon-HaCaT) were treated similarly, and protein expression was analyzed by Western blot.

Article Snippet: The following primary antibodies were used for immunoblotting: Grp78 (Santa Cruz, SC-13968), KRT1 (Abclonal, A9776), IVL (Abclonal, A8026), Ki67 (Abcam, ab16667), XBP1s (Abclonal, A17007), XBP1u (Proteintech, 25997-1-AP), PERK (Proteintech, 24390-1-AP), p-PERK (Abclonal, AP1501), ATF6 (Proteintech, 24169-1-AP), β-Actin (Santa Cruz, sc-47778).

Techniques: Transfection, shRNA, Control, Expressing, Western Blot

Journal: Antioxidants

Article Title: CHIP Haploinsufficiency Exacerbates Hepatic Steatosis via Enhanced TXNIP Expression and Endoplasmic Reticulum Stress Responses

doi: 10.3390/antiox12020458

Figure Lengend Snippet: CHIP is involved in unfolded protein responses (UPRs) and apoptosis in hepatocytes. ( a ) AML12 cells were transfected with control (siControl) or CHIP siRNA (siCHIP) for 48 h and then treated with tunicamycin (TM, 5 or 10 μM) for 24 h. Protein levels of GRP78, ATF6, XBP-1s and CHIP were determined by immunoblotting. A-tubulin was used as a loading control. ( b ) AML12 cells were transfected with siControl or siCHIP for 48 h and then treated with TM (10 μM) for 24 h. Protein levels of cleaved PARP-1, cleaved caspase-3 (cleaved Casp3), and CHIP were determined by immunoblotting. α-tubulin was used as a loading control. ( c ) AML12 cells were transfected with siControl or siCHIP for 48 h and then treated with TM (10 μM) for 24 h. Expression of UPR-related genes were measured by qRT-PCR. Relative expression levels were normalized to GAPDH levels. ** p < 0.01 vs. siControl, ## p < 0.01 vs. siCHIP, † p < 0.05 and †† p < 0.01. ( d ) Primary hepatocytes from CHIP +/+ , CHIP +/− , and CHIP −/− mice were treated with TM (2 or 10 μM) for 6 h. Protein levels of GRP78, CHOP, XBP-1s, and CHIP were measured by immunoblotting. β-actin was used as a loading control. ( e ) Primary hepatocytes from CHIP +/+ and CHIP +/− mice were treated with brefeldin A (BFA, 1 or 2 μM) for 6 or 9 h. Protein levels of GRP78, CHOP, cleaved PARP-1, and CHIP were measured by immunoblotting. α-tubulin was used as a loading control.

Article Snippet: The antibodies were purchased from the following vendors: TXNIP (MBL International, Woburn, MA, USA); KDEL (GRP94, GRP78) (Enzo Life Sciences, Lörrach, Germany); XBP-1s (BioLegend, San Diego, CA, USA); ATF6 (Novus Biologicals, Littleton, CO, USA); ATF4, GADD153 (CHOP), HA, and CHIP (Santa Cruz Biotechnology, Santa Cruz, CA, USA); Akt, p-Akt, ACC, FAS, PARP-1, and cleaved Caspase-3 (Cell Signaling, Danvers, MA, USA); NLRP3 (ThermoFisher, Waltham, MA, USA); PGC1α (abcam, Cambridge, UK); and α-tubulin and β-actin (Sigma Aldrich, St. Louis, MO, USA).

Techniques: Transfection, Control, Western Blot, Expressing, Quantitative RT-PCR, ChIP-chip

Journal: Shock

Article Title: Endoplasmic Reticulum Stress Pathway Involvement in Local and Remote Myocardial Ischemic Conditioning

doi: 10.1097/shk.0b013e31828e4f80

Figure Lengend Snippet: FIG. 3. Western blot analysis of GRP78 (A) and ATF6 50 kd (B) at 15-min reperfusion in LV homogenates from rat hearts subjected to I/R. Top, Example of immunoblots of GRP78 and GAPDH (A), cleaved ATF6 and GAPDH (B). Bottom, Bar graphs showing means T SEM of the densitometry of GRP78- to-GAPDH ratio (A) and ATF6 50 kd-to-GAPDH ratio (B). *P G0.05 vs. control; UP G 0.05 vs. RIPer; n = 6 in each group.

Article Snippet: D ow nloaded from http://journals.lw w .com /shockjournal by B hD M f5eP H K av1zE oum 1tQ fN 4a+ kJLhE Z gbsIH o4X M i0h C yw C X 1A W nY Q p/IlQ rH D 3i3D 0O dR yi7T vS F l4C f3V C 4/O A V pD D a8K K G K V 0Y m y+ 78= on 09/03/2024 (pH 7.6), and 0.1% Tween-20, the membranes were incubated overnight at 4-C with goat antibody against GRP78 (1/1,000; Santa Cruz Biotechnology, Santa Cruz, Calif) and mouse antibody against ATF6 (1/500, IMGENEX).

Techniques: Western Blot, Control

Journal: Shock

Article Title: Endoplasmic Reticulum Stress Pathway Involvement in Local and Remote Myocardial Ischemic Conditioning

doi: 10.1097/shk.0b013e31828e4f80

Figure Lengend Snippet: FIG. 5. Western blot analysis of GRP78 (A) and ATF6 50 kd (B) at 15-min reperfusion in LV homogenates from rat hearts subjected to I/R in the presence of 4-PBA. Top, Example of immunoblots of GRP78 and GAPDH (A) and cleaved ATF6 and GAPDH (B). Bottom, Bar graphs showing means T SEM of the densitometry of GRP78-to-GAPDH ratio (A), ATF6 50 kd-to-GAPDH ratio (B). No significant difference between groups; n = 5Y6 in each group.

Article Snippet: D ow nloaded from http://journals.lw w .com /shockjournal by B hD M f5eP H K av1zE oum 1tQ fN 4a+ kJLhE Z gbsIH o4X M i0h C yw C X 1A W nY Q p/IlQ rH D 3i3D 0O dR yi7T vS F l4C f3V C 4/O A V pD D a8K K G K V 0Y m y+ 78= on 09/03/2024 (pH 7.6), and 0.1% Tween-20, the membranes were incubated overnight at 4-C with goat antibody against GRP78 (1/1,000; Santa Cruz Biotechnology, Santa Cruz, Calif) and mouse antibody against ATF6 (1/500, IMGENEX).

Techniques: Western Blot

Journal: Shock

Article Title: Hepatic Apoptosis Postburn Is Mediated by C-Jun N-Terminal Kinase 2

doi: 10.1097/shk.0b013e31827f40ab

Figure Lengend Snippet: FIG. 2. Hepatic ER stress was initiated after burn in both wild-type and JNK2 knockout (JNK2j/j) mice. Bip (A) and activated ATF6 (B) levels were quantified 1, 3, and 5 days after burn relative to "-actin. Representative blots from sham and burn groups at day 1 are shown above each graph. Downstream effectors of ER stress were transcribed in wild-type mice but not JNK2 knockout mice, as indicated by mRNA expression of XBP1s, Pdia3, and Dnajb9 (CYE) measured by real time PCR of day 5 liver samples. Data presented are mean T SEM. *P G 0.05 and ***P G 0.001 vs. sham.

Article Snippet: The antibody against mouse ATF6 was purchased from Imgenex (San Diego, Calif).

Techniques: Knock-Out, Expressing, Real-time Polymerase Chain Reaction