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nupr1 polyclonal antibody (Bioss)

Name: nupr1 polyclonal antibody
Brand: Bioss
Rating: 94 (8 reviews)

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Bioss nupr1 polyclonal antibody
Nupr1 Polyclonal Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/nupr1 polyclonal antibody/product/Bioss
Average 94 stars, based on 8 article reviews

nupr1 polyclonal antibody - by Bioz Stars, 2026-02

94/100 stars

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Palmitate activates the PERK branch of UPR signaling and increases the expression of Nupr1 in human chondrocytes. (A) Human chondrocytes were stimulated with 500 μM BSA-conjugated palmitate or oleate overnight and probed for CHOP, Nupr1, TRB3, and CC3 antibodies, respectively. Inhibitors (1 nM of PERKi or 60 nM of 4μ8C) were added to the cells 1 h prior to the treatments as needed. Blots were stripped and reprobed with GAPDH as a loading control. Densitometric analyses for protein levels of CHOP (B), Nupr1 (C), TRB3 (D), and CC3 (E) were performed on blots obtained in three independent experiments similar to the one shown in panel A. (F) Human chondrocytes were stimulated with 500 μM BSA-conjugated palmitate or oleate overnight. The protein lysates obtained were assessed by co-immunoprecipitation with a Nupr1-specific antibody, and the Nupr1-associated proteins were then probed for TRB3 antibody. Densitometric analyses for protein levels of TRB3 (G) were performed on blots obtained from three independent experiments similar to the one shown in panel F. Data are shown as mean ± standard deviation of the mean. Ctrl, Control; Palm, Palmitate; Ole., Oleate.

Journal: FASEB journal : official publication of the Federation of American Societies for Experimental Biology

Article Title: Nuclear protein-1 is the common link for pathways activated by aging and obesity in chondrocytes: A potential therapeutic target for osteoarthritis

doi: 10.1096/fj.202201700RR

Figure Lengend Snippet: Palmitate activates the PERK branch of UPR signaling and increases the expression of Nupr1 in human chondrocytes. (A) Human chondrocytes were stimulated with 500 μM BSA-conjugated palmitate or oleate overnight and probed for CHOP, Nupr1, TRB3, and CC3 antibodies, respectively. Inhibitors (1 nM of PERKi or 60 nM of 4μ8C) were added to the cells 1 h prior to the treatments as needed. Blots were stripped and reprobed with GAPDH as a loading control. Densitometric analyses for protein levels of CHOP (B), Nupr1 (C), TRB3 (D), and CC3 (E) were performed on blots obtained in three independent experiments similar to the one shown in panel A. (F) Human chondrocytes were stimulated with 500 μM BSA-conjugated palmitate or oleate overnight. The protein lysates obtained were assessed by co-immunoprecipitation with a Nupr1-specific antibody, and the Nupr1-associated proteins were then probed for TRB3 antibody. Densitometric analyses for protein levels of TRB3 (G) were performed on blots obtained from three independent experiments similar to the one shown in panel F. Data are shown as mean ± standard deviation of the mean. Ctrl, Control; Palm, Palmitate; Ole., Oleate.

Article Snippet: The following antibodies were used for immunohistochemistry: rabbit polyclonal anti-Nupr1 (bs-7106R from Bioss); rabbit monoclonal anti-CC3 (9664 from Cell Signaling Technology), and rabbit monoclonal anti-MMP3 (ab52915 from Abcam).

Techniques: Expressing, Control, Immunoprecipitation, Standard Deviation

Oxidation of IRE1 induces Nupr1 and MMP production in human chondrocytes. (A) Human chondrocytes were treated with 25 μM of menadione for 0, 15, 30, 60,90, and 120 min, respectively, and probed for P-IRE1(Y628 or S724), total IRE1(T-IRE1), XBP1s, Nupr1, Nrf2, P-p38, and total p38 (T-p38) antibodies, respectively. (B) Human chondrocytes treated with 25 μM of menadione for 0-120 min were assessed for IRE-1:SOH by immunoblot. Densitometric analyses for protein levels of IRE-1:SOH (C) were performed on blots obtained from three independent experiments similar to the one shown in panel B. Data are shown as mean ± standard deviation of the mean. (D) Human chondrocytes were treated with 25 μM of menadione for 0 and 30 min, and probed for P-IRE1(Y628 or S724), T-IRE1, XBP1s, Nupr1, Nrf2, P-p38, and T-p38 antibodies, respectively. Inhibitors (10 μM of p38i or 60 nM of 4μ8C were added to the cells 1 h prior to the treatments as needed. (E) Human chondrocytes were transfected with control siRNA or siRNA specific for nupr1, and then treated with 25 μM of menadione overnight and probed for Nupr1, P-IRE1 (Y628), XBP1s, and Nrf2, respectively. Conditioned medium was probed for MMP3 and ADAMTS5. (F) Human chondrocytes were treated with 25 μM of menadione overnight and probed for P-IRE1(Y628 or S724), XBP1s, Nupr1, Nrf2, ATF4, CHOP, and cytochrome C (CytoC) respectively. Conditioned medium was probed for MMP3 and ADAMTS5. Inhibitors (60 nM of 4μ8C or 1 mM of PBA) were added into the cells 1 h prior to the treatments as needed. Blots were stripped and reprobed with GAPDH as a loading control. For conditioned medium, blots were stripped and reprobed with ADAMTS5 as a loading control.

Journal: FASEB journal : official publication of the Federation of American Societies for Experimental Biology

Article Title: Nuclear protein-1 is the common link for pathways activated by aging and obesity in chondrocytes: A potential therapeutic target for osteoarthritis

doi: 10.1096/fj.202201700RR

Figure Lengend Snippet: Oxidation of IRE1 induces Nupr1 and MMP production in human chondrocytes. (A) Human chondrocytes were treated with 25 μM of menadione for 0, 15, 30, 60,90, and 120 min, respectively, and probed for P-IRE1(Y628 or S724), total IRE1(T-IRE1), XBP1s, Nupr1, Nrf2, P-p38, and total p38 (T-p38) antibodies, respectively. (B) Human chondrocytes treated with 25 μM of menadione for 0-120 min were assessed for IRE-1:SOH by immunoblot. Densitometric analyses for protein levels of IRE-1:SOH (C) were performed on blots obtained from three independent experiments similar to the one shown in panel B. Data are shown as mean ± standard deviation of the mean. (D) Human chondrocytes were treated with 25 μM of menadione for 0 and 30 min, and probed for P-IRE1(Y628 or S724), T-IRE1, XBP1s, Nupr1, Nrf2, P-p38, and T-p38 antibodies, respectively. Inhibitors (10 μM of p38i or 60 nM of 4μ8C were added to the cells 1 h prior to the treatments as needed. (E) Human chondrocytes were transfected with control siRNA or siRNA specific for nupr1, and then treated with 25 μM of menadione overnight and probed for Nupr1, P-IRE1 (Y628), XBP1s, and Nrf2, respectively. Conditioned medium was probed for MMP3 and ADAMTS5. (F) Human chondrocytes were treated with 25 μM of menadione overnight and probed for P-IRE1(Y628 or S724), XBP1s, Nupr1, Nrf2, ATF4, CHOP, and cytochrome C (CytoC) respectively. Conditioned medium was probed for MMP3 and ADAMTS5. Inhibitors (60 nM of 4μ8C or 1 mM of PBA) were added into the cells 1 h prior to the treatments as needed. Blots were stripped and reprobed with GAPDH as a loading control. For conditioned medium, blots were stripped and reprobed with ADAMTS5 as a loading control.

Techniques: Western Blot, Standard Deviation, Transfection, Control

Menadione upregulates Nupr1 expression at the post-translational level. Human chondrocytes were treated with 25 μM of menadione overnight; total RNA was isolated, cDNA was synthesized, and qRT-PCR was performed using primers specific for nupr1 (A), CHOP (B), and TRB3 (C). Data were normalized to TBP as a control and shown as mean ± standard deviation of the mean (n = 3). (D) Human chondrocytes were treated with 25 μM of menadione for 0, 15, 30, 60,90, and 120 min, respectively, and assessed by co-immunoprecipitation with a Nupr1-specific antibody, and the Nupr1-associated proteins were then probed with P-Thr/Ser, and ubiquitin antibodies, respectively. (E) Human chondrocytes were treated with 25 μM of menadione for 0 or 15 min, and assessed by co-immunoprecipitation with a Nupr1-specific antibody, and the Nupr1-associated proteins were then probed with P-Thr/Ser, and ubiquitin antibodies, respectively. Inhibitors (10 μM of p38i or 60 nM of 4μ8C) were added to the cells 1 h prior to the treatments as needed.

Journal: FASEB journal : official publication of the Federation of American Societies for Experimental Biology

Article Title: Nuclear protein-1 is the common link for pathways activated by aging and obesity in chondrocytes: A potential therapeutic target for osteoarthritis

doi: 10.1096/fj.202201700RR

Figure Lengend Snippet: Menadione upregulates Nupr1 expression at the post-translational level. Human chondrocytes were treated with 25 μM of menadione overnight; total RNA was isolated, cDNA was synthesized, and qRT-PCR was performed using primers specific for nupr1 (A), CHOP (B), and TRB3 (C). Data were normalized to TBP as a control and shown as mean ± standard deviation of the mean (n = 3). (D) Human chondrocytes were treated with 25 μM of menadione for 0, 15, 30, 60,90, and 120 min, respectively, and assessed by co-immunoprecipitation with a Nupr1-specific antibody, and the Nupr1-associated proteins were then probed with P-Thr/Ser, and ubiquitin antibodies, respectively. (E) Human chondrocytes were treated with 25 μM of menadione for 0 or 15 min, and assessed by co-immunoprecipitation with a Nupr1-specific antibody, and the Nupr1-associated proteins were then probed with P-Thr/Ser, and ubiquitin antibodies, respectively. Inhibitors (10 μM of p38i or 60 nM of 4μ8C) were added to the cells 1 h prior to the treatments as needed.

Techniques: Expressing, Isolation, Synthesized, Quantitative RT-PCR, Control, Standard Deviation, Immunoprecipitation

Genetic deletion of Nupr1 reduces the severity of cartilage lesions in a mouse model of post-traumatic OA. Experimental OA was induced by DMM surgery in the left knee joints of wild-type (WT) and Nupr1−/− mice. After 8 weeks, knee joints were then collected, processed, and sectioned for histologic analyses. (A) Hematoxylin and eosin staining showing less OA-like changes in the knee joints of Nupr1−/− mice. In the WT (Nupr1+/+) DMM mouse joint shown at the top, there is a prominent osteophyte (score = 3/3) at the medial (left) abaxial site. In the Nupr1−/− mouse shown below, a small osteophyte (score = 1/3) is present. (B) Percentage of area of articular cartilage occupied by dead chondrocytes. (C) Osteophyte score at the medial tibial plateau (MTP). (D) ACS score at the MTP. (E) Articular cartilage thickness is measured at the medial tibial plateau (MTP) (n = 3/genotype) as shown. (F) Mouse knee joint sections were analyzed immunohistochemically for Nupr1, CC3, and MMP3. Images on left in each set of panels are of low magnification (Scale bars: 100 μm), and the tibia is in the lower half of the images. The areas inside the small rectangles are magnified and displayed in the panels on the right (scale bars: 20 μm). All immunohistochemical data were quantified with corrections for cell numbers and statistically analyzed.

Journal: FASEB journal : official publication of the Federation of American Societies for Experimental Biology

Article Title: Nuclear protein-1 is the common link for pathways activated by aging and obesity in chondrocytes: A potential therapeutic target for osteoarthritis

doi: 10.1096/fj.202201700RR

Figure Lengend Snippet: Genetic deletion of Nupr1 reduces the severity of cartilage lesions in a mouse model of post-traumatic OA. Experimental OA was induced by DMM surgery in the left knee joints of wild-type (WT) and Nupr1−/− mice. After 8 weeks, knee joints were then collected, processed, and sectioned for histologic analyses. (A) Hematoxylin and eosin staining showing less OA-like changes in the knee joints of Nupr1−/− mice. In the WT (Nupr1+/+) DMM mouse joint shown at the top, there is a prominent osteophyte (score = 3/3) at the medial (left) abaxial site. In the Nupr1−/− mouse shown below, a small osteophyte (score = 1/3) is present. (B) Percentage of area of articular cartilage occupied by dead chondrocytes. (C) Osteophyte score at the medial tibial plateau (MTP). (D) ACS score at the MTP. (E) Articular cartilage thickness is measured at the medial tibial plateau (MTP) (n = 3/genotype) as shown. (F) Mouse knee joint sections were analyzed immunohistochemically for Nupr1, CC3, and MMP3. Images on left in each set of panels are of low magnification (Scale bars: 100 μm), and the tibia is in the lower half of the images. The areas inside the small rectangles are magnified and displayed in the panels on the right (scale bars: 20 μm). All immunohistochemical data were quantified with corrections for cell numbers and statistically analyzed.

Techniques: Staining, Immunohistochemical staining

Model showing critical role of Nupr1 in obesity, aging, and injury-linked OA pathogenesis. →, single-step stimulation; → →, multistep stimulations; big and bold arrow, dominant stimulation; ⊥ ⊥, multistep inhibitions; knockdown of calnexin; ROS, reactive oxygen species; BIP, binding immunoglobulin protein.

Journal: FASEB journal : official publication of the Federation of American Societies for Experimental Biology

Article Title: Nuclear protein-1 is the common link for pathways activated by aging and obesity in chondrocytes: A potential therapeutic target for osteoarthritis

doi: 10.1096/fj.202201700RR

Figure Lengend Snippet: Model showing critical role of Nupr1 in obesity, aging, and injury-linked OA pathogenesis. →, single-step stimulation; → →, multistep stimulations; big and bold arrow, dominant stimulation; ⊥ ⊥, multistep inhibitions; knockdown of calnexin; ROS, reactive oxygen species; BIP, binding immunoglobulin protein.

Techniques: Knockdown, Binding Assay

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