No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Rat (Rattus) MAP3K1 Antibodies:
anti-Mouse (Murine) MAP3K1 Antibodies:
anti-Human MAP3K1 Antibodies:
Go to our pre-filtered search.
Human Polyclonal MAP3K1 Primary Antibody for DB, ELISA - ABIN537663
Mokhtari, Myers, Welsh: MAPK kinase kinase-1 is essential for cytokine-induced c-Jun NH2-terminal kinase and nuclear factor-kappaB activation in human pancreatic islet cells. in Diabetes 2008
let-7g induces porcine granulosa cells apoptosis by inhibiting the MAP3K1 gene, which promotes FoxO1 expression and dephosphorylation with nuclear accumulation.
Data identify a unique signal crosstalk between Wnt signaling and the MAP3K1-JNK pathway in epithelial morphogenesis.
These results reveal the importance of the MEKK1-calponin-3 signaling pathway to cell contractility.
Map3k1 regulates iNKT cell proliferative expansion in response to glycolipid antigen
goya and kinase-deficient Map3k1 homozygotes initially develop supernumerary cochlear outer hair cells (OHCs) that subsequently degenerate.
These data highlight the crucial role of MAP3K1 in the development and function of the mouse inner ear and hearing.
Dioxin exposure markedly inhibited c-Jun phosphorylation in Map3k1-deficient embryonic eyelid epithelium, suggesting that dioxin-induced AHR pathways can synergize with gene mutations to inhibit MAP3K1 signaling.
Both the MEKK1 PHD and TAB1 are critical for ES-cell differentiation
Results suggest that proto-oncogene protiins c-Jun and mitogen-activated protein 3 kinase 1 (MAP3K1) represent parallel pathways in the control of eyelid closure.
Aberrant expression of Map3k1 enabled growth factor-autonomous proliferation and drove BRAF-independent ERK signaling, thus shedding light on alternative means of activating this prominent signaling pathway in melanoma.
analysis of the gene expression program of MAP3K1 in mouse eyelid morphogenesis
Proximal to the RING domain is a SWIM (SWI2/SNF2 and MuDR) domain. The MEKK1 SWIM domain, but not the RING domain, directly associates with the c-Jun DNA-binding domain, and the SWIM domain is required for MEKK1-dependent c-Jun ubiquitylation.
MAP3K1 is the nexus of an intracrine regulatory loop connecting the TGF-alpha/EGFR/RhoA-c-Jun and JNK-c-Jun-AP-1 pathways in developmental eyelid closure.
MAP3K1 is not required for mouse testis determination
A novel role for MAP3K1 in which it crosstalks with the cell cycle regulatory pathways in the prevention of retina malformation and degeneration.
MEK kinase 1: kinase domain deficiency in mice reveals a role in orchestrating the thymus-dependent immunity and TNFR family signaling
It was suggested that a high predisposition to catalepsy in mice can be defined by the Map3k1, Il6st, Gzmk, and Hspb3 genes' coexpression network.
MAP/ERK kinase kinase 1 (MEKK1) mediates transcriptional repression by interacting with polycystic kidney disease-1 (PKD1) promoter-bound p53 tumor suppressor protein
Data suggest that Map3k1 is the most probable candidate mutant gene of B6-Co mice.
MEK kinase 1 induces mitochondrial permeability transition leading to apoptosis
caspase cleavage of MEKK1 is a dynamic regulatory mechanism that alters the subcellular distribution of MEKK1, changing its function to pro-apoptotic signaling
Tyrosine to phenylalanine mutations decrease phosphorylation of the substrate MAP kinase kinase 1 (MKK1), suggesting the important role of this residue in the regulation of MAP kinase kinase kinase 1 (MEKK1) kinase activity.
double mekk1/camta3 mutant positioned CAMTA3 downstream of MEKK1 and verified their distinct roles in GSR regulation. mekk1-5 displays programmed cell death and overaccumulates reactive oxygen species and salicylic acid
Treatment of Arabidopsis with a membrane rigidifier, DMSO, causes MPK4 activation concomitantly with MEKK1 and MKK2 phosphorylation.
Ca(2+) signaling occurred upstream of the MEKK1-MKK2 pathway. MEKK1 was phosphorylated by calcium/calmodulin-regulated receptor-like kinase (CRLK1), which suggested that CRLK1 is one of candidates located upstream of MEKK1.
MEKK1 plays a key role in transducing the l-Glu signal that elicits large-scale changes in root architecture, and provide genetic evidence for the existence in plants of an external glutamate (l-Glu) signalling pathway analogous to that found in animals.
Data indicate that MEKK2 is required for the mekk1, mkk1 mkk2, and mpk4 autoimmune phenotypes.
Data suggest that the MEKK1-MKK1/MKK2-MPK4 kinase cascade negatively regulates MEKK2 and activation of MEKK2 triggers SUMM2-mediated immune responses.
CRLK1 interacts with MEKK1 in vitro and in planta during cold treatment.
An analysis of the interation of MEKK1 and MEK1 in response to wounding stress in A. thaliana seedlings is presented.
MEKK1 is essential for activation of MPK4 and negatively regulates temperature-sensitive and tissue-specific cell death and H(2)O(2) accumulation that are dependent on both RAR1 (resistance protein function) and SID2 (isochorismate synthase)
This study demonstrated that analysis of plants carrying T-DNA knockout alleles indicated that MEKK1 is required for flg22-induced activation of MPK4.
Treatment with elevated levels of sodium chloride improves the growth of mekk1 transgenic plants;the mekk1;mpk4 double-mutant combination causes seedling lethality.
MEKK1 is a bifunctional protein: it binds to the promoter of the WRKY53 gene regulating the switch from a leaf age dependent to a plant age dependent expression
Activation of MPK4 by flg22 is impaired in the mkk1 mkk2 double mutants, suggesting that MKK1 and MKK2 function together with MPK4 and MEKK1 in a MAP kinase cascade to negatively regulate innate immune responses in plants.
Of note, the enforced expression of MEKK1 or the exposure of medulloblastoma cells to the MEKK1 activator, Nocodazole, resulted in a marked inhibitory effect on GLI1 activity and tumor cell proliferation and viability. Taken together, the results of this study shed light on a novel regulatory mechanism of HH signaling, with potentially relevant implications in cancer therapy.
CXCL12 activates the MEKK1/JNK signaling pathway, which in turn initiates SMAD3 phosphorylation, its translocation to nuclei, and recruitment of SMAD3 to the CTGF promoter, which ultimately induces CTGF expression in human lung fibroblasts.
Through a stratification analysis, 5q11.2/MAP3K1 (rs16886034, rs16886364, rs16886397, rs1017226, rs16886448) and 7q32.3/LINC-PINT (rs4593472) were associated with Luminal A, and 10q26.1/FGFR2 (rs35054928) was associated with Luminal B.
findings show a robust association between the variant allele of rs832582 (MAP3K1906Val) and decreased VFDs in patients with ARDS and suggest that this variant may predispose individuals to a greater inflammatory response.
We have revealed significant association of FGFR2 and MAP3K1 polymorphisms with breast cancer.
Identification of a MAP3K1 variant should prompt an evaluation for disorders of sex development in female siblings of the proband
Polymorphism of MAP3K1 is associated with breast cancer.
SNP variants at the MAP3K1/SETD9 gene boundary associate with somatic PIK3CA variants in breast cancers.
CSN6 positively regulates c-Jun in a MEKK1-dependent manner
Mekk1 mediates p53 protein stability in the presence of Mdm2 and reduces p53 ubiquitination, suggesting an interference with Mdm2-mediated degradation of p53 by the ubiquitin-proteasome pathway.
BAALC conferred chemoresistance in acute myeloid leukemia cells by upregulating ATP-binding cassette proteins in an ERK-dependent manner, which can be therapeutically targeted by MEK inhibitor
MiR-451 inhibited the proliferation of esophageal squamous cell carcinoma cells by targeting CDKN2D and MAP3K1 expression.
There were 3 specimens with mutations in MAP3K1 (MEKK1), including two truncation mutants, T779fs and T1481fs; T1481fs encoded an unstable and nonfunctional protein when expressed in vitro.
Single nucleotide polymorphisms in ALDOB, MAP3K1, and MEF2C are associated with cataract.
Results demonstrate that MAP3K1 rs889312 is closely correlated with outcome among diffuse-type gastric cancer in a Chinese population.
We propose that the cancer risk alleles act to increase MAP3K1 expression in vivo and might promote breast cancer cell survival.
The present meta-analysis suggests that MAPKKK1 rs889312-C allele and rs16886165-G allele might be risk factors for breast cancer, especially in Europeans and Asians.
MAP3K1 mutations tilt the balance in the sex-determining pathways by downregulating SOX9 and FGF9.
MAP3K1 protein expression level in breast cancer cells was higher than that in normal mammary gland cells.
MAP3K1 single nucleotide polymorphism rs889312 was confirmed to be associated with breast cancer risk (P = 0.04, OR 1.15, 95% CI 1.01-1.30).
The protein encoded by this gene is a serine/threonine kinase and is part of some signal transduction cascades, including the ERK and JNK kinase pathways as well as the NF-kappa-B pathway. The encoded protein is activated by autophosphorylation and requires magnesium as a cofactor in phosphorylating other proteins. This protein has E3 ligase activity conferred by a plant homeodomain (PHD) in its N-terminus and phospho-kinase activity conferred by a kinase domain in its C-terminus.
mitogen-activated protein kinase kinase kinase 1
, MAPK/ERK kinase kinase 1
, MEK kinase 1
, MEKK 1
, mitogen activated protein kinase kinase kinase 1
, MAP/ERK kinase kinase 1