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anti-Human CAMKK2 Anticorps:
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Human Polyclonal CAMKK2 Primary Antibody pour IF (p), IHC (p) - ABIN716426
Zhao, Zhang, Liu, Zhang, Hao, Li, Chen, Shen, Tang, Min, Meng, Wang, Yi, Zhang: Hydrogen Sulfide and/or Ammonia Reduces Spermatozoa Motility through AMPK/AKT Related Pathways. dans Scientific reports 2016
Show all 3 Pubmed References
Human Monoclonal CAMKK2 Primary Antibody pour ELISA, WB - ABIN524083
Kou, Sartoretto, Michel: Regulation of Rac1 by simvastatin in endothelial cells: differential roles of AMP-activated protein kinase and calmodulin-dependent kinase kinase-beta. dans The Journal of biological chemistry 2009
Human Monoclonal CAMKK2 Primary Antibody pour IP, ELISA - ABIN564643
Karacosta, Foster, Azabdaftari, Feliciano, Edelman: A regulatory feedback loop between Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2) and the androgen receptor in prostate cancer progression. dans The Journal of biological chemistry 2012
Human Polyclonal CAMKK2 Primary Antibody pour ICC, IF - ABIN4287593
Massie, Lynch, Ramos-Montoya, Boren, Stark, Fazli, Warren, Scott, Madhu, Sharma, Bon, Zecchini, Smith, Denicola, Mathews, Osborne, Hadfield, Macarthur, Adryan, Lyons, Brindle, Griffiths, Gleave et al.: The androgen receptor fuels prostate cancer by regulating central metabolism and biosynthesis. ... dans The EMBO journal 2011
Human Polyclonal CAMKK2 Primary Antibody pour IP, WB - ABIN950067
Krishan, Richardson, Sahni: The Anticancer Agent, Di-2-Pyridylketone 4,4-Dimethyl-3-Thiosemicarbazone (Dp44mT), Up-Regulates the AMPK-Dependent Energy Homeostasis Pathway in Cancer Cells. dans Biochimica et biophysica acta 2016
CAMKK2 and AMPK have opposing effects on lipogenesis, providing a potential mechanism for their contrasting effects on prostate cancer progression in vivo
Inhibition of AMPK with Compound C prevents the TNFalpha-induced activatory phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser1177 and reduces the NO release. AMPK is activated by phosphorylation catalysed by liver kinase B1 (LKB1) and calcium/calmodulin-dependent protein kinase kinase beta (CaMKKbeta), which are phosphorylated and thereby activated in the presence of TNFalpha.
CaMKK2 is found to be expressed in both breast cancer cells and within stromal cells. CaMKK2 expression inversely correlated with the less aggressive luminal A (LA) molecular type, and a trend for higher CaMKK2 expression in triple-negative TN type was also observed.
Studied inhibition by herbal preparation HX109 of androgen receptors thru calcium/calmodulin dependent protein kinase kinase 2 (CAMKK2)/activating transcription factor 3 (ATF3) signal pathways in prostate cancer cell line; also found HX109 to ameliorate testosterone propionate induced benign prostate hyperplasia thru androgen receptor inhibition.
Silencing of TRPC5 and inhibition of autophagy reverses adriamycin drug resistance in breast carcinoma via CaMKKbeta/AMPKalpha/mTOR pathway.
results demonstrated that SSd induces autophagy through the CaMKKbeta-AMPK-mTOR signalling pathway in Autosomal dominant polycystic kidney disease (ADPKD) cells, indicating that SSd might be a potential therapy for ADPKD and that SERCA might be a new target for ADPKD treatment.
Three single nucleotide polymorphisms (SNPs) within P2X4R and two SNPs within CAMKK2 influenced concentrations of TNFalpha in peripheral blood mononuclear cells, but these SNP did not associate with risk for HIV-associated sensory neuropathy in South Africans.
Serum CAMKK2 was downregulated in female schizophrenic patients compared with female healthy individuals.
This study provides insight into functionally disruptive, rare-variant mutations in human CaMKK2, which have the potential to influence risk and burden of disease associated with aberrant CaMKK2 activity in human populations carrying these variants.
14-3-3gamma protein directly interacts with the kinase domain of CaMKK2 and the region containing the inhibitory phosphorylation site Thr(145) within the N-terminal extension. CaMKK isoforms differ in their 14-3-3-mediated regulations and the interaction between 14-3-3 protein and the N-terminal 14-3-3-binding motif of CaMKK2 might be stabilized by small-molecule compounds.
CAMKK2 exhibited the strongest associations with HIV-associated sensory neuropathy (HIV-SN), with two SNPs and six haplotypes predicting SN status in black Southern Africans.
Study used three cognitive tasks and fMRI to provide convergent evidence of a link between the rs1063843 SNP of CAMKK2 and the function of the dorsolateral prefrontal cortex. In addition, this polymorphism was associated with the function of the striatum during a working memory task.
Data suggest that CAMKK2 is highly expressed in high-grade ovarian cancer and ovarian cancer cell lines; CAMKK2 directly activates Akt1 by phosphorylation at Thr-308 in a Ca2+/calmodulin-dependent manner; CAMKK2 knockdown or inhibition decreases Akt1 phosphorylation at Thr-308 and Ser-473. (CAMKK2 = calcium/calmodulin dependent protein kinase kinase 2; AKT1 = AKT serine/threonine kinase 1)
Single nucleotide polymorphism in CAMKK2 gene is associated with pulmonary non-tuberculous mycobacterial disease.
This study showed that the expression level of CAMKK2 could be regulated by promoter methylation. CAMKK2 serves as a prognostic marker in gliomas and could be a potential therapeutic target in gliomas.
For the first time, we showed that rs1063843, a single nucleotide polymorphism located in the CAMKK2 gene, is highly associated with bipolar disorder
Site-directed mutagenesis analysis revealed that Leu(358) in CaMKKbeta/Ile(322) in CaMKKalpha confer, at least in part, a distinct recognition of AMPK but not of CaMKIalpha.
Clopidogrel diminishes TNFalpha-stimulated VCAM-1 expression at least in part via HO-1 induction and CaMKKbeta/AMPK/Nrf2 pathway in endothelial cells.
CaMKK2 (and Nup62) are required for optimal androgen receptor transcriptional activity in castrate resistant prostate cancer cells.
Silencing of CAMKK2 using siRNA significantly reduced cell proliferation, colony formation and invasion of gastric cancer cells.
the data presented here underscore the therapeutic potential of targeting CaMKK2 to promote efficacious and rapid healing of bone fractures and as a mechanism to strengthen normal bones.
These data provide a valuable resource by establishing criteria for use of STO-609 to inhibit the in vivo functions of CaMKK2 and demonstrate its utility for treating metabolically-related hepatic disease.
CaMKK2 is highly expressed within intratumoral myeloid cells in mouse models of breast cancer, and demonstrate its inhibition within myeloid cells suppresses tumor growth by increasing intratumoral accumulation of effector CD8(+) T cells and immune-stimulatory myeloid subsets. Tumor-associated macrophages isolated from Camkk2 KO mice expressed higher levels of chemokines involved in the recruitment of effector T cells.
we demonstrated that systemic administration of the small molecule CaMKK2 inhibitor, STO-609, to irradiated mice enhanced Hematopoietic stem and progenitor cells (HSPCs)recovery and improved survival. These findings identify CaMKK2 as an important regulator of HSPC regeneration and demonstrate CaMKK2 inhibition is a novel approach to promoting hematopoietic recovery after BM injury.
loss of blood-brain barrier proteins, inactivation of survival gene expression such as B-cell lymphoma 2 (Bcl-2) and an increase in inflammatory cytokines in the serum were observed after stroke with CaMKK beta inhibition. We demonstrate that CaMKK beta is neuroprotective in stroke in aged mice
CaMKK2 as a molecular rheostat for insulin action.
CaMKK2 Inhibits C2C12 Myoblasts Proliferation and Differentiation through AMPK. Overexpression of CaMKK2 Inhibits Muscle Regeneration in Vivo.
In summary, we demonstrate a new mechanism of calcium dependent antibacterial strategy in E. coli infected macrophages, which requires autophagy enhancement mediated by activation of CaMKKbeta, ERK, AMPK and FoxO1.
CaMKKbeta exerts protective effects on cardiac adaptive energy pooling against pressure-overload possibly through phosphorylation of AMPK and by upregulation of PGC-1alpha.
Results demonstrated that genetically inhibiting the CaMKK pathway via CaMKKbeta or CaMK IV is detrimental in the response of female mice to cerebral ischemia
a novel function for CaMKK2 in bone remodeling and highlight the potential for its therapeutic inhibition as a valuable bone anabolic strategy that also inhibits OC differentiation in the treatment of osteoporosis.
Flow-enhanced sirtuin (SIRT)1 stability is primarily mediated by CaMKKbeta phosphorylation of sirtuin SIRT1 at Ser-27 and Ser-47.
amino acid starvation regulates autophagy in part through an increase in cellular Ca(2+) that activates a CaMKK-beta-AMPK pathway and inhibits mTORC1, which results in ULK1 stimulation
Results suggest that in PCa progression, CaMKK2 and the AR are in a feedback loop in which CaMKK2 is induced by the AR to maintain AR activity, AR-dependent cell cycle control, and continued cell proliferation.
an important function for CaMKK2 in mediating mechanisms that control the amplitude of macrophage inflammatory responses to excess nutrients or pathogen derivatives
Suppressed catecholamine-induced induction of gluconeogenic gene expression in CaMKK2 knockout mice leads to improved whole-body glucose homeostasis despite the presence of increased hepatic fat content.
a novel role for CaMKK2 as an inhibitor of granulocytic fate commitment and differentiation in early myeloid progenitors
conclude that CaMKK2 and AMP-activated protein kinase function in a signaling pathway that participates in the regulation of adiposity
findings suggest CaM kinase kinase beta isoforms are required for the formation of hippocampal long-term memory[LTM], but not needed for contextual, trace fear, and passive avoidance LTM
Taken together, we conclude that CaMKKbeta has a male-specific function in hippocampal memory formation and we have identified male-restricted transcription occurring during hippocampal memory formation.
the expression, but not the kinase activity, of AMPK and CaMKKbeta is necessary for ADP signaling to eNOS
The product of this gene belongs to the Serine/Threonine protein kinase family, and to the Ca(2+)/calmodulin-dependent protein kinase subfamily. The major isoform of this gene plays a role in the calcium/calmodulin-dependent (CaM) kinase cascade by phosphorylating the downstream kinases CaMK1 and CaMK4. Protein products of this gene also phosphorylate AMP-activated protein kinase (AMPK). This gene has its strongest expression in the brain and influences signalling cascades involved with learning and memory, neuronal differentiation and migration, neurite outgrowth, and synapse formation. Alternative splicing results in multiple transcript variants encoding distinct isoforms. The identified isoforms differ in their ability to undergo autophosphorylation and to phosphorylate downstream kinases.
CAMKK beta protein
, caM-KK 2
, caM-KK beta
, caM-kinase kinase 2
, caM-kinase kinase beta
, calcium/calmodulin-dependent protein kinase beta
, calcium/calmodulin-dependent protein kinase kinase 2
, caMKK 2
, caMKK beta
, calcium/calmodulin-dependent protein kinase kinase beta
, calcium/calmodulin-dependent protein kinase (CaM kinase) II beta 1
, protein-tyrosine kinase
, calcium/calmodulin-dependent protein kinase II beta
, calcium/calmodulin-dependent protein kinase kinase 2, beta
, calcium/calmodulin-dependent protein kinase kinase 2-like
, Ca+/Calmodulin-dependent protein kinase kinase beta (CaM-kinase kinase beta)
, CaM-kinase kinase beta
, calcium/calmodulin-dependent protein kinase 2 beta