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Human Monoclonal TRIM32 Primary Antibody für IF, RNAi - ABIN524889
Schwamborn, Berezikov, Knoblich: The TRIM-NHL protein TRIM32 activates microRNAs and prevents self-renewal in mouse neural progenitors. in Cell 2009
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Human Polyclonal TRIM32 Primary Antibody für ICC, IF - ABIN443593
Fatima, Kumari, Schwamborn, Mahadevan, Shankar, Raja, Seth: Tripartite containing motif 32 modulates proliferation of human neural precursor cells in HIV-1 neurodegeneration. in Cell death and differentiation 2016
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Cow (Bovine) Polyclonal TRIM32 Primary Antibody für WB - ABIN2780865
Chiang, Beck, Yen, Tayeh, Scheetz, Swiderski, Nishimura, Braun, Kim, Huang, Elbedour, Carmi, Slusarski, Casavant, Stone, Sheffield: Homozygosity mapping with SNP arrays identifies TRIM32, an E3 ubiquitin ligase, as a Bardet-Biedl syndrome gene (BBS11). in Proceedings of the National Academy of Sciences of the United States of America 2006
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Human Polyclonal TRIM32 Primary Antibody für ELISA, WB - ABIN564975
Sato, Okumura, Iguchi, Ariga, Hatakeyama: TRIM32 promotes retinoic acid receptor ?-mediated differentiation in human promyelogenous leukemic cell line HL60. in Biochemical and biophysical research communications 2012
TRIM32 as a crucial positive regulator of Herpes Simplex Virus type 1 (HSV-1) induced IFN-beta (zeige IFNB1 Antikörper) production in corneal epithelial cells, and it played a predominant role in clearing HSV-1 from the cornea.
HSP70 (zeige HSP70 Antikörper)-TRIM32 complex is biochemically distinct from the previously characterized 14-3-3 (zeige YWHAQ Antikörper)-TRIM32 phospho-complex.
Data suggest that, in cardiomyocytes, TRIM32 attenuates activation of SRF signaling and hypertrophy due to dysbindin; TRIM24 promotes these effects. TRIM32 promotes dysbindin degradation; TRIM24 protects dysbindin from degradation. (TRIM = tripartite motif-containing protein; SRF = serum response factor)
Duchenne muscular dystrophy (zeige DMD Antikörper) muscles showed a selective up-regulation of the ubiquitin ligase tripartite motif-containing protein 32 (TRIM32). The induction of TRIM32 was due to a transcriptional effect and it correlated with disease severity.
we provide a detailed characterization of the TRIM (zeige TRAT1 Antikörper) ligases TRIM25 (zeige TRIM25 Antikörper) and TRIM32 and show how their oligomeric state is linked to catalytic activity
that TRIM32 plays a protective role in aortic banding-induced pathological cardiac remodelling by blocking Akt (zeige AKT1 Antikörper)-dependent signalling
these findings suggest that TRIM32 might play important roles in the hepatocarcinogenesis.
results show a novel molecular cascade involving miR (zeige MLXIP Antikörper)-155 and TRIM32 leading to HIV-1 Tat (zeige TAT Antikörper)-induced attenuated proliferation of neural precursor cells; study also uncovered an unidentified role for miR (zeige MLXIP Antikörper)-155 in modulating human neural stem cell proliferation, helping in better understanding of neural precursor cells and diseased brain
Studies indicate most-studied TRIpartite Motif (TRIM (zeige TRAT1 Antikörper))-NHL (zeige RTEL1 Antikörper) proteins TRIM2 (zeige TRIM2 Antikörper), TRIM3 (zeige TRIM3 Antikörper), TRIM32 and TRIM71 (zeige TRIM71 Antikörper), and their mutations have been linked to diseases.
Results suggest that Salmonella effector SseK3 binding to host tripartite motif-containing 32 protein (TRIM32) in the inhibition of nuclear factor kappa B (NF-kappaB (zeige NFKB1 Antikörper)) activation: [SseK3]
suppression of Trim32 promotes the recovery of neurological function after traumatic brain injury.
the presented data link the Parkinson's disease-associated gene alpha-synuclein to the neuronal cell fate determinant TRIM32.
TRIM32 is a novel essential positive factor modulating axonal regeneration and the recovery of motor function following SCI, possibly through suppressing proliferation of glial cells.
TRIM32 protein expression is defective in atopic dermatitis lesional skin.
In summary, the data presented here reveal that TRIM32 directly regulates at least two of the four Yamanaka Factors (cMyc (zeige MYC Antikörper) and Oct4 (zeige POU5F1 Antikörper)), to modulate cell fate transitions.
TRIM32 represents a model of intrinsic immunity, in which a host protein directly senses and counters viral infection in a species specific fashion by directly limiting viral replication
NDRG2 (zeige NDRG2 Antikörper) accumulated in skeletal muscle and myoblasts in the absence of TRIM32. NDRG2 (zeige NDRG2 Antikörper) overexpression in myoblasts led to reduced cell proliferation and delayed cell cycle withdrawal during differentiation.
TRIM32 overexpression promotes cell oncogenic transformation and tumorigenesis in mice in a largely p53 (zeige TP53 Antikörper)-dependent manner.
The protein encoded by this gene is a member of the tripartite motif (TRIM) family. The TRIM motif includes three zinc-binding domains, a RING, a B-box type 1 and a B-box type 2, and a coiled-coil region. The protein localizes to cytoplasmic bodies. The protein has also been localized to the nucleus, where it interacts with the activation domain of the HIV-1 Tat protein. The Tat protein activates transcription of HIV-1 genes.
E3 ubiquitin-protein ligase TRIM32
, tripartite motif-containing 32
, TAT-interactive protein, 72-KD
, tripartite motif containing 32
, 72 kDa Tat-interacting protein
, tripartite motif-containing protein 32
, zinc finger protein HT2A
, zinc-finger protein HT2A
, bM468K2.2 (tripartite motif protein 32)
, tripartite motif protein 32
, zinc finger protein 117