Immunohistochemistry analysis of JNK1 showing staining in the cytoplasm of paraffin-embedded human prostate carcinoma (right) compared to a negative control without primary antibody (left). To expose target proteins, antigen retrieval was performed using 10mM sodium citrate (pH 6.0), microwaved for 8-15 min. Following antigen retrieval, tissues were blocked in 3% H2O2-methanol for 15 min at room temperature, washed with ddH2O and PBS, and then probed with a JNK1 Rabbit Polyclonal Antibody (44690G) diluted in 3% BSA-PBS at a dilution of 1:100 overnight at 4°C in a humidified chamber. Tissues were washed extensively in PBST and detection was performed using an HRP-conjugated secondary antibody followed by colorimetric detection using a DAB kit. Tissues were counterstained with hematoxylin and dehydrated with ethanol and xylene to prep for mounting.
|Tested species reactivity||Human, Mouse, Rat|
|Published species reactivity||Non-human primate, Human, Not Applicable|
|Host / Isotype||Rabbit / IgG|
|Immunogen||The antiserum was produced against a chemically synthesized peptide derived from an internal region of JNK1. This region is conserved among human, mouse, and rat forms of JNK1, JNK2, and JNK3 proteins.|
|Purification||Antigen affinity chromatography|
|Storage buffer||Dulbecco's PBS, pH 7.3, with 1mg/ml BSA, 50% glycerol|
|Contains||0.05% sodium azide|
|Tested Applications||Dilution *|
|Flow Cytometry (Flow)||1:20|
|Immunohistochemistry (Paraffin) (IHC (P))||1:20-1:200|
|Western Blot (WB)||1:500|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
C-Jun N-terminal Kinase (JNK) is also known as Mitogen-activated protein kinase (MAPK8). It belongs to the MAPK superfamily of stress-activated protein kinases. MAPKs are Serine-threonine protein kinases that are activated in response to a variety of extracellular stimuli, and mediate signal transduction from the cell surface to the nucleus. JNK is involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation and development. JNK pathways are activated by stress and inflammatory signals. JNK is expressed as ten different isoforms due to differential mRNA splicing. The predominant forms are JNK1 and JNK2.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Expression of cFLIPL Determines the Basal Interaction of Bcl-2 With Beclin-1 and Regulates p53 Dependent Ubiquitination of Beclin-1 During Autophagic Stress.
44-690G was used in western blot to study regulation of p53 dependent ubiquitination of Beclin-1 during autophagic stress and basal interaction of Bcl-2 with Beclin-1 by expression of cFLIPL
|Ranjan K,Pathak C||Journal of cellular biochemistry (117:1757)||2016|
FADD regulates NF-¿B activation and promotes ubiquitination of cFLIPL to induce apoptosis.
44-690G was used in western blot to show how FADD regulates NF-kappaB activation and promotes ubiquitination of cFLIPL, which induces apoptosis
|Ranjan K,Pathak C||Scientific reports (6:null)||2016|
|Non-human primate||Not Cited||
Functional comparison of herpes simplex virus 1 (HSV-1) and HSV-2 ICP27 homologs reveals a role for ICP27 in virion release.
44-690G was used in western blot to compare ICP27t2 and ICP27 from herpes simplex virus
|Park D,Lalli J,Sedlackova-Slavikova L,Rice SA||Journal of virology (89:2892)||2015|
Imatinib restores VASP activity and its interaction with Zyxin in BCR-ABL leukemic cells.
44-690G was used in western blot to study the effect of Imatinib on VASP activity and its interaction with Zyxin in BCR-ABL leukemic cells.
|Bernusso VA,Machado-Neto JA,Pericole FV,Vieira KP,Duarte AS,Traina F,Hansen MD,Olalla Saad ST,Barcellos KS||Biochimica et biophysica acta (1853:388)||2015|
Increased ERK and JNK activation and decreased ERK/JNK ratio are associated with long-term organ damage in patients with systemic lupus erythematosus.
44-690G was used in western blot to test if extracellular signal-regulated kinase and c-Jun N-terminal kinase are associated with long-term organ damage in SLE patients.
|Bloch O,Amit-Vazina M,Yona E,Molad Y,Rapoport MJ||Rheumatology (Oxford, England) (53:1034)||2014|
|Human||Not Cited||Molecular pathway profiling of T lymphocyte signal transduction pathways; Th1 and Th2 genomic fingerprints are defined by TCR and CD28-mediated signaling.||Smeets RL,Fleuren WW,He X,Vink PM,Wijnands F,Gorecka M,Klop H,Bauerschmidt S,Garritsen A,Koenen HJ,Joosten I,Boots AM,Alkema W||BMC immunology (13:null)||2012|
|Not Applicable||Not Cited||
Varicella-zoster virus infection of human fibroblast cells activates the c-Jun N-terminal kinase pathway.
44-690G was used in western blot to study the effect of infection with varicella-zoster virus on c-Jun N-terminal kinase signaling
|Zapata HJ,Nakatsugawa M,Moffat JF||Journal of virology (81:977)||2007|
|Human||Not Cited||The mitogen-activated protein kinases (MAPK) p38 and JNK are markers of tumor progression in breast carcinoma.||Davidson B,Konstantinovsky S,Kleinberg L,Nguyen MT,Bassarova A,Kvalheim G,Nesland JM,Reich R||Gynecologic oncology (102:453)||2006|
|Human||Not Cited||Matrix metalloproteinases (MMP), EMMPRIN (extracellular matrix metalloproteinase inducer) and mitogen-activated protein kinases (MAPK): co-expression in metastatic serous ovarian carcinoma.||Davidson B,Givant-Horwitz V,Lazarovici P,Risberg B,Nesland JM,Trope CG,Schaefer E,Reich R||Clinical and experimental metastasis (20:621)||2003|
Homozygous deletion of MKK4 in ovarian serous carcinoma.
44-690G was used in immunohistochemistry - paraffin section to search for chromosomal deletions in ovarian serous carcinoma and identify genes that could contribute to disease
|Nakayama K,Nakayama N,Davidson B,Katabuchi H,Kurman RJ,Velculescu VE,Shih IeM,Wang TL||Cancer biology and therapy (5:630)||2006|