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-Human Adenylate Kinase 2 Antibodies:
anti-Mouse (Murine) Adenylate Kinase 2 Antibodies:
anti-Rat (Rattus) Adenylate Kinase 2 Antibodies:
Go to our pre-filtered search.
Adenylate kinase 2 deficiency limits survival and regulates various genes during larval stages of Drosophila melanogaster.
Data demonstrate that adenylate kinase 2 plays a critical role in adenine nucleotide metabolism in the mitochondrial intermembrane space and is essential for growth.
Reticular dysgenesis-associated AK2 protects hematopoietic stem and progenitor cell development from oxidative stress.
Knockdown of zebrafish ak2 also leads to aberrant leukocyte development, stressing the evolutionarily conserved role of AK2.
Genetic variants of AK2 activates tenofovir for HIV therapy.
Reticular dysgenesis -patient derived induced pluripotent stem cells can recapitulate disease phenotype which can be rescued by AK2 overexpression.
In conclusion, our data suggest that SIRPalpha signaling through SHP-2-PI3K-Akt2 strongly influences osteoblast differentiation from bone marrow stromal cells.
AK2 deficiency compromises the mitochondrial energy metabolism required for differentiation of human neutrophil and lymphoid lineages.
results suggest that AK2 is an associated activator of DUSP26 and suppresses cell proliferation by FADD dephosphorylation, postulating AK2 as a negative regulator of tumour growth.
AK2 is indispensable for neutrophil differentiation, indicating a possible causative link between AK2 deficiency and neutropenia in reticular dysgenesis.
These results suggest that, acting in concert with FADD and caspase-10, AK2 mediates a novel intrinsic apoptotic pathway that may be involved in tumorigenesis.
The alpha-borano or alpha-H on PMEA and PMPA were detrimental to the activity of recombinant human AMP kinases 2
Biallelic mutations in AK2 (adenylate kinase 2) in seven individuals affected with reticular dysgenesis and sensorineural deafness, were identified.
The gene encoding the mitochondrial energy metabolism enzyme adenylate kinase 2 (AK2) is mutated in individuals with reticular dysgenesis.
In addition to AK1 and AK2, which we previously demonstrated are present in outer dense fibers and mitochondrial sheath of the mouse sperm tail, we show that another AK, AK8, is present in a third flagellar compartment, the axoneme.
Adenylate kinase 2 links mitochondrial energy metabolism to the induction of the unfolded protein response.
Reduced Akt2 leads to up-regulation of Rab4a expression in cardiomyocytes in a cell-autonomous fashion that may involve activation of PPARalpha.
AK2 in the flagellar accessory structures provides a mechanism to buffer the adenylate energy charge for sperm motility. Ak2 protein was localized to the mitochondrial sheath in the sperm midpiece.
Adenylate kinases are involved in regulating the adenine nucleotide composition within a cell by catalyzing the reversible transfer of phosphate groups among adenine nucleotides. Three isozymes of adenylate kinase, namely 1, 2, and 3, have been identified in vertebrates\; this gene encodes isozyme 2. Expression of these isozymes is tissue-specific and developmentally regulated. Isozyme 2 is localized in the mitochondrial intermembrane space and may play a role in apoptosis. Mutations in this gene are the cause of reticular dysgenesis. Alternate splicing results in multiple transcript variants. Pseudogenes of this gene are found on chromosomes 1 and 2.
, adenylate kinase-2
, adenylate kinase 2
, AK 2
, ATP-AMP transphosphorylase 2
, ATP:AMP phosphotransferase
, adenylate kinase 2, mitochondrial
, adenylate monophosphate kinase
, adenylate kinase isoenzyme 2, mitochondrial
, adenylate kinase isozyme 2