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The natural substrate for this enzyme may be peptidyl- tRNAs which drop off the ribosome during protein synthesis (By similarity). Additionally we are shipping Peptidyl-tRNA Hydrolase 2 Antibodies (87) and many more products for this protein.
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These collective findings indicate that loss of Bit1 expression contributes to the acquisition of malignant phenotype of human lung epithelial cells via Erk (show EPHB2 Proteins) activation-induced suppression of E-cadherin (show CDH1 Proteins) expression.
This study reports on five infantile-onset multisystem neurologic, endocrine, and pancreatic disease (IMNEPD) patients with a different homozygous PTRH2 mutation, broaden the phenotypic spectrum of the disease and differentiate common symptoms and interindividual variability in IMNEPD associated with a unique mutation.
Homozygous mutation in PTRH2 gene causes progressive sensorineural deafness and peripheral neuropathy in three sisters from a consanguineous family.
Bcl-2 (show BCL2 Proteins) expression patterns in various differentiated esophageal squamous cell carcinoma were higher than those in corresponding normal esophageal tissues with no statistical differences ( p > 0.05). Importantly, Bit1 expression was positively correlated with both matrix metalloproteinase 2 (show MMP2 Proteins) and Bcl-2 (show BCL2 Proteins) expression in esophageal squamous cell carcinoma and esophageal adenocarcinoma tissues ( p < 0.05).
Our data establishes a PTRH2 mutation as a n (show DMD Proteins)ovel driver of (show DMD Proteins) congenital muscle degeneration and identifies a potential novel target to treat muscle (show DMD Proteins) myopathies.
Bit1 may be an important regulator in cell growth, apoptosis, migration and invasion of esophageal squamous cell carcinoma via targeting FAK (show PTK2 Proteins)-paxillin (show PXN Proteins) pathway.
these findings suggest a tumor suppressive role of the caspase-independent anoikis effector Bit1 in lung cancer.
Reduction of the Bit1 level in cytosol, regulated by E2 binding to ESR1 (show ESR1 Proteins), was mainly mediated through PI3K (show PIK3CA Proteins)/AKT (show AKT1 Proteins) pathways.
Bit1 plays pivotal roles in the development and progression of ESCC, and its biological functions in ESCC may be closely associated with AIF (show AIFM1 Proteins) and Bcl-2 (show BCL2 Proteins) levels.
TLE1 (show TLE1 Proteins) inhibits the Bit1 anoikis pathway by reducing the formation of the proapoptotic Bit1-AES (show AES Proteins) complex in part through sequestration of AES (show AES Proteins) in the nucleus.
Ptrh2 levels were up-regulated in dystrophin (show DMD Proteins) deficient mdx (show DMD Proteins) muscle, which correlates with the elevated levels of the a7b1 integrin observed in mdx (show DMD Proteins) muscle and Duchenne muscular dystrophy (show DMD Proteins) patients. Similar to the a7 integrin, Ptrh2 expression was decreased in laminin-a2 null gastrocnemius muscle
These results support an unanticipated yet essential role for Bit-1 in controlling myogenesis through regulation of Bcl-2 (show BCL2 Proteins).
downregulation of Bit1 specifically potentiated tumor metastasis in vivo
Bit-1 mediates integrin-dependent cell survival through activation of the NFkappaB pathway
These studies establish the physiological significance of Bit1 activity and begin to delineate a Bit1 signaling pathway that acts through Erk (show EPHB2 Proteins) regulation.
The natural substrate for this enzyme may be peptidyl- tRNAs which drop off the ribosome during protein synthesis (By similarity).
peptidyl-tRNA hydrolase 2
, PTH 2
, bcl-2 inhibitor of transcription 1
, peptidyl-tRNA hydrolase 2, mitochondrial
, Bcl-2 inhibitor of transcription