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Phospho-p38 MAPK (Thr180/Tyr182) (12F8) Rabbit mAb antibody


Antibody ID


Target Antigen

Phospho-p38 MAPK (Thr180/Tyr182) (12F8) Rabbit mAb drosophila/arthropod, other mammalian, human, non-human primate, mouse, rat, zebrafish/fish, hamster, h, m, r, mk, dm, (hm, mi, z)

Proper Citation

(Cell Signaling Technology Cat# 4631, RRID:AB_331765)


monoclonal antibody


Applications: W, IHC-P, IF-IC. Consolidation on 11/2018: AB_10078335, AB_10080263, AB_10104828, AB_331765, AB_331766.

Host Organism



Cell Signaling Technology

Gain-of-Function Mutation of Card14 Leads to Spontaneous Psoriasis-like Skin Inflammation through Enhanced Keratinocyte Response to IL-17A.

  • Wang M
  • Immunity
  • 2018 Jun 28

Literature context:


Genetic mutations of CARD14 (encoding CARMA2) are observed in psoriasis patients. Here we showed that Card14E138A/+ and Card14ΔQ136/+ mice developed spontaneous psoriasis-like skin inflammation, which resulted from constitutively activated CARMA2 via self-aggregation leading to the enhanced activation of the IL-23-IL-17A cytokine axis. Card14-/- mice displayed attenuated skin inflammation in the imiquimod-induced psoriasis model due to impaired IL-17A signaling in keratinocytes. CARMA2, mainly expressed in keratinocytes, associates with the ACT1-TRAF6 signaling complex and mediates IL-17A-induced NF-κB and MAPK signaling pathway activation, which leads to expression of pro-inflammatory factors. Thus, CARMA2 serves as a key mediator of IL-17A signaling and its constitutive activation in keratinocytes leads to the onset of psoriasis, which indicates an important role of NF-κB activation in keratinocytes in psoriatic initiation.

Funding information:
  • NIGMS NIH HHS - R01 GM28896(United States)

Inhibition of A-Type K+ Channels by Urotensin-II Induces Sensory Neuronal Hyperexcitability Through the PKCα-ERK Pathway.

  • Zhang Y
  • Endocrinology
  • 2018 May 1

Literature context:


Previous studies have implicated urotensin-II in the nociception of sensory neurons. However, to date the relevant mechanisms remain unknown. In the current study we determined the role of urotensin-II in the regulation of transient outward A-type potassium currents (IA) and neuronal excitability in trigeminal ganglion (TG) neurons. We found that application of urotensin-II to small-diameter TG neurons decreased IA in a dose-dependent manner, whereas the delayed rectifier potassium current was unaffected. The IA decrease induced by urotensin-II depended on the urotensin-II receptor (UT-R) and was associated with a hyperpolarizing shift in the steady-state inactivation curve. Exposure of TG cells to urotensin-II markedly increased protein kinase C (PKC) activity, and PKC inhibition eliminated the UT-R-mediated IA decrease. Antagonism of PKCα, either pharmacologically or genetically, but not of PKCβ prevented the decrease in IA induced by urotensin-II. Analysis of phospho-extracellular signal-regulated kinase (p-ERK) revealed that urotensin-II significantly increased the expression level of p-ERK, whereas p-p38 and p-c-Jun N-terminal kinase remained unchanged. Inhibition of mitogen-activated protein kinase/ERK signaling by the kinase antagonist U0126 and PD98059 completely abolished the UT-R-mediated IA decrease. Moreover, urotensin-II significantly increased the action potential firing rate of small TG neurons; pretreatment with 4-aminopyridine prevented this effect. In summary, our findings suggest that urotensin-II selectively attenuated IA through stimulation of the PKCα-dependent ERK1/2 signaling pathway. This UT-R-dependent mechanism might contribute to neuronal hyperexcitability in TG neurons.

Funding information:
  • NCI NIH HHS - P01CA130818(United States)

IL-1β Upregulates StAR and Progesterone Production Through the ERK1/2- and p38-Mediated CREB Signaling Pathways in Human Granulosa-Lutein Cells.

  • Dang X
  • Endocrinology
  • 2017 Oct 1

Literature context:


The proinflammatory cytokine interleukin-1β (IL-1β) may be involved in several ovulation-associated events, such as protease synthesis, prostaglandin production, and steroidogenesis in granulosa cells. However, the exact effect of IL-1β on progesterone synthesis in granulosa cells and the underlying mechanism remain unclear. By using cultured granulosa-lutein cells collected from women undergoing in vitro fertilization or intracytoplasmic sperm injection, we found that IL-1β upregulated steroidogenic acute regulatory protein (StAR) expression and progesterone synthesis in granulosa-lutein cells, which was comparable with luteinizing hormone effect and could be abolished by an IL-1 receptor antagonist. Moreover, IL-1β activated the phosphorylation of cyclic adenosine monophosphate response element-binding protein (CREB), and knockdown of CREB attenuated the induction of StAR expression and progesterone synthesis by IL-1β in granulosa-lutein cells. Furthermore, IL-1β activated the extracellular signal-regulated kinase (ERK)1/2 and p38 pathways and inhibition of the ERK1/2 and p38 pathways attenuated the IL-1β-induced phosphorylation of CREB, StAR expression, and progesterone synthesis in granulosa-lutein cells. In conclusion, IL-1β could upregulate StAR expression and stimulate progesterone biosynthesis through increase in CREB phosphorylation via activating the ERK1/2 and p38 pathways in human granulosa-lutein cells.

Dexmedetomidine prolongs levobupivacaine analgesia via inhibition of inflammation and p38 MAPK phosphorylation in rat dorsal root ganglion.

  • Yamakita S
  • Neuroscience
  • 2017 Oct 11

Literature context:


Following tissue injury, phosphorylation of p38 MAPK in the primary afferent neurons drives sensitization of peripheral nerve. Dexmedetomidine extends the duration of reginal analgesia by local anesthetics. The effect of regional analgesia on the peripheral nerve sensitization is not known. The aim of this study is to investigate the effect of regional analgesia by levobupivacaine with or without dexmedetomidine on the p38 MAPK phosphorylation in the dorsal root ganglion (DRG) and inflammatory reaction in the peripheral tissue. A plantar incision was made in the hind paws of Sprague-Dawley rats. Prior to incision, levobupivacaine with or without dexmedetomidine was injected to the plantar aspect of the paws and ankles. A behavioral study was performed to investigate pain hypersensitivity. Phosphorylation of p38 MAPK in the DRG was assessed by immunohistochemistry and Western blotting. Macrophage accumulation, NGF, and TNF-α in the DRG and plantar tissue were measured using immunohistochemistry, real-time PCR and ELISA. Pain hypersensitivity was induced immediately after the plantar incision. Treatment with levobupivacaine inhibited the development of pain hypersensitivity for two hours. Adjunctive dexmedetomidine extended the anti-hyperalgesic duration for four hours. Levobupivacaine without dexmedetomidine could not inhibit p38 MAPK phosphorylation in the DRG completely. However, Levobupivacaine and dexmedetomidine completely inhibited p38 MAPK phosphorylation, and reduced macrophage accumulation and TNF-α amount in the plantar tissue. Inhibition of p38 MAPK phosphorylation via TNF-α suggests dexmedetomidine has a peripheral mechanism of anti-inflammatory action when used asan adjunct to local anesthetics, and provides a molecular basis for the prevention of peripheral sensitization following surgery.

Glial activation in the periaqueductal gray promotes descending facilitation of neuropathic pain through the p38 MAPK signaling pathway.

  • Ni HD
  • J. Neurosci. Res.
  • 2016 Jan 28

Literature context:


The midbrain ventrolateral periaqueductal gray (VL-PAG) is a key component that mediates pain modulation. Although spinal cord glial cells appear to play an important role in chronic pain development, the precise mechanisms involving descending facilitation pathways from the PAG following nerve injury are poorly understood. This study shows that cellular events that occur during glial activation in the VL-PAG may promote descending facilitation from the PAG during neuropathic pain. Chronic constriction nerve injury (CCI) was induced by ligature construction of the sciatic nerve in male Sprague-Dawley rats. Behavioral responses to noxious mechanical (paw withdrawal threshold; PWT) and thermal (paw withdrawal latency; PWL) stimuli were evaluated. After CCI, immunohistochemical and Western blot analysis of microglia and astrocytes in the VL-PAG showed morphological and quantitative changes indicative of activation in microglia and astrocytes. Intra-VL-PAG injection of microglial or astrocytic inhibitors attenuated PWT and PWL at days 7 and 14, respectively, following CCI. We also evaluated the effects of intra-VL-PAG administration of the phosphorylated p38 mitogen-activated protein kinase (p-p38 MAPK) inhibitor SB 203580 at day 7 after CCI. This treatment abolished microglial activation and produced a significant time-dependent attenuation of PWT and PWL. Western blot analysis showed localized expression of p-p38 in the VL-PAG after CCI. P-p38 was expressed in labeled microglia of the VL-PAG but was not present in astrocytes and neurons on day 7 after CCI. These results demonstrate that CCI-induced neuropathic pain is associated with glial activation in the VL-PAG, which likely participates in descending pain facilitation through the p38 MAPK signaling pathway.

Funding information:
  • NCI NIH HHS - CA173903(United States)