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抗Rat (Rattus) PTK2B 抗体:
抗Mouse (Murine) PTK2B 抗体:
抗Human PTK2B 抗体:
Human Monoclonal PTK2B Primary Antibody for ICS - ABIN1177156
Anand, Cucchiarini, Terwilliger, Ganju: The tyrosine kinase Pyk2 mediates lipopolysaccharide-induced IL-8 expression in human endothelial cells. in Journal of immunology (Baltimore, Md. : 1950) 2008
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Human Monoclonal PTK2B Primary Antibody for ICS - ABIN1177155
Avraham, Park, Schinkmann, Avraham: RAFTK/Pyk2-mediated cellular signalling. in Cellular signalling 2000
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Human Monoclonal PTK2B Primary Antibody for IHC, ELISA - ABIN1724705
Dylla, Deyle, Theunissen, Padurean, Verfaillie: Integrin engagement-induced inhibition of human myelopoiesis is mediated by proline-rich tyrosine kinase 2 gene products. in Experimental hematology 2004
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Human PTK2B Primary Antibody for IHC - ABIN966926
Gluck: Acid sensing in renal epithelial cells. in The Journal of clinical investigation 2004
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Human Polyclonal PTK2B Primary Antibody for IF, IHC - ABIN362858
Benzing, Gerke, Höpker, Hildebrandt, Kim, Walz: Nephrocystin interacts with Pyk2, p130(Cas), and tensin and triggers phosphorylation of Pyk2. in Proceedings of the National Academy of Sciences of the United States of America 2001
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Human Polyclonal PTK2B Primary Antibody for ICC, IF - ABIN257536
Lu, Chen, Shimoda, Park, Zhang, Tran, Zhang, Semenza: Chemotherapy-Induced Ca(2+) Release Stimulates Breast Cancer Stem Cell Enrichment. in Cell reports 2017
Cow (Bovine) Polyclonal PTK2B Primary Antibody for WB - ABIN2779801
Ling, Sheng, Braun: The calcium-dependent activity of large-conductance, calcium-activated K+ channels is enhanced by Pyk2- and Hck-induced tyrosine phosphorylation. in American journal of physiology. Cell physiology 2004
Human Polyclonal PTK2B Primary Antibody for IF (p), IHC (p) - ABIN745118
Cao, Zheng, Wang, Wang, Li, Li, Lai, Wang, Qin: Src blockage by siRNA inhibits VEGF-induced vascular hyperpemeability and osteoclast activity - an in vitro mechanism study for preventing destructive repair of osteonecrosis. in Bone 2015
Tideglusib significantly reduced cerebral infarct volume at both 24h and 7days after HI injury. Tideglusib also increased phosphorylated GSK-3beta (显示 GSK3b 抗体)(Ser9) and Akt (显示 AKT1 抗体)(Ser473)
Therefore our study identifies a compartmentalized PtdIns(3,4,5)P3/AKT (显示 AKT1 抗体)/GSK3beta (显示 GSK3b 抗体) signaling axis at cilia in SHH (显示 SHH 抗体)-dependent medulloblastoma that is regulated by INPP5E (显示 INPP5E 抗体) to maintain tumor cell cilia, promote SHH (显示 SHH 抗体) signaling and thereby medulloblastoma progression.
mTORC2 (显示 CRTC2 抗体) complex is responsible for phosphorylating Akt (显示 AKT1 抗体) at S(473).
FHL2 (显示 FHL2 抗体) facilitates ovarian granulosa cell tumor progression via controlling AKT1 (显示 AKT1 抗体) transcription.
Omentin (显示 ITLN1 抗体) protects against lipopysaccharides-induced acute respiratory distress syndrome through suppressing pulmonary inflammation and promoting endothelial barrier via an Akt (显示 AKT1 抗体)/NOS3 (显示 NOS3 抗体)-dependent mechanism.
AIM2 (显示 AIM2 抗体) contributes to the maintenance of intestinal integrity via Akt (显示 AKT1 抗体) and protects against Salmonella mucosal infection.
Following transepithelial migration, neutrophils adhesion to ICAM-1 (显示 ICAM1 抗体) resulted in activation of Akt (显示 AKT1 抗体) and beta-catenin (显示 CTNNB1 抗体) signaling, increased epithelial-cell proliferation, and wound healing.
Besides, both in vivo and in votro studies suggested that K145 stimulated insulin (显示 INS 抗体) dependent Akt (显示 AKT1 抗体) phosphorylation and subsequently activates FoxO1 (显示 FOXO1 抗体) phosphorylation therefore inhibited gluconeogenetic genes expression including PEPCK (显示 PEPCK 抗体) and G6pase (显示 G6PC 抗体). Our study figures out a potential extent increase the value of developing K145 as therapeutic candidate for diabetes.
C5a in vitro caused activation (phosphorylation) of MAPKs and Akt (显示 AKT1 抗体) in cardiomyocytes, which required availability of both C5a receptors. These data suggest that polymicrobial sepsis causes cardiac dysfunction that appears to be linked to activation of MAPKs and Akt (显示 AKT1 抗体) in heart.
High Akt1 (显示 AKT1 抗体) expression is associated with hepatocarcinogenesis.
Our findings suggest that Pyk2 plays an important role in the coordination of stabilization of beta-catenin (显示 CTNNB1 抗体) in the crosstalk between Wnt (显示 WNT2 抗体)/beta-catenin (显示 CTNNB1 抗体) and Wnt (显示 WNT2 抗体)/Ca(2 (显示 CA2 抗体)+) signaling pathways upon Wnt3a (显示 WNT3A 抗体) stimulation in differentiating hNPCs.
STIM1 (显示 STIM1 抗体)-induced Ca(2 (显示 CA2 抗体)+) signaling activates Pyk2 to inhibit the interaction of VE-PTP (显示 PTPRB 抗体) and VE-cadherin (显示 CDH5 抗体) and hence increase endothelial permeability.
Ascites and CCL18 (显示 CCL18 抗体) stimulate the phosphorylation and expression of Pyk2, which positively regulates ascites-induced ovarian cancer cell migration.
We demonstrated trophoblast cytoprotection by intervention with supraphysiological concentrations of relaxin, a process in part mediated through the PI3-kinase (显示 PIK3CA 抗体)-Akt/PKB (显示 AKT1 抗体) cell survival pathway. These results provide further rationale for clinical investigation of relaxin as a potential therapeutic in preeclampsia.
PTK2B polymorphism (rs28834970) could modify the risk of late-onset Alzheimer's disease (LOAD), and PTK2B polymorphism (rs28834970) and APOE may interact to increase LOAD risk in a Han Chinese population.
Studies suggest that PYK2 is a common downstream effector of ErbB (显示 EGFR 抗体) and IL8 (显示 IL8 抗体) receptors, and that PYK2 integrates their signaling pathways through a positive feedback loop to potentiate breast cancer invasion.
Pyk2 is a key downstream signaling molecules of CCR7 (显示 CCR7 抗体) in SCCHN, which promotes SCCHN tumorigenesis and progression.
Phosphoproteomic analysis identifies FAK2 as a potential therapeutic target for tamoxifen resistance in breast cancer.
Pyk2-focal adhesion targeting domain interacts with and binds to leupaxin (显示 LPXN 抗体).
Src (显示 SRC 抗体) has a role in priming Pyk2 (but not FAK (显示 PTK2 抗体)) phosphorylation and subsequent activation downstream of integrins
Ptk2b activation may play a key role in the signaling responses in ECs under hemodynamic influence [proline-rich tyrosine kinase 2]
This gene encodes a cytoplasmic protein tyrosine kinase which is involved in calcium-induced regulation of ion channels and activation of the map kinase signaling pathway. The encoded protein may represent an important signaling intermediate between neuropeptide-activated receptors or neurotransmitters that increase calcium flux and the downstream signals that regulate neuronal activity. The encoded protein undergoes rapid tyrosine phosphorylation and activation in response to increases in the intracellular calcium concentration, nicotinic acetylcholine receptor activation, membrane depolarization, or protein kinase C activation. This protein has been shown to bind CRK-associated substrate, nephrocystin, GTPase regulator associated with FAK, and the SH2 domain of GRB2. The encoded protein is a member of the FAK subfamily of protein tyrosine kinases but lacks significant sequence similarity to kinases from other subfamilies. Four transcript variants encoding two different isoforms have been found for this gene.
, PKB alpha
, RAC protein kinase alpha RAC-PK alpha
, RAC-alpha serine/threonine-protein kinase
, murine thymoma viral (v-akt) oncogene homolog 1
, protein kinase B alpha
, thymoma viral proto-oncogene 1
, protein kinase B-alpha
, proto-oncogene c-AKT
, related to A and C kinases
, FADK 2
, PTK2B protein tyrosine kinase 2 beta
, calcium-dependent tyrosine kinase
, calcium-regulated non-receptor proline-rich tyrosine kinase
, cell adhesion kinase beta
, focal adhesion kinase 2
, proline-rich tyrosine kinase 2
, protein kinase B
, protein-tyrosine kinase 2-beta
, related adhesion focal tyrosine kinase
, CAK beta
, PTK2 protein tyrosine kinase 2 beta
, cellular adhesion kinase beta
, protein tyrosine kinase 2 beta