rabbit anti palb2 antibody  (Proteintech)

Journal: EMBO Reports

Article Title: Arginine methylation-dependent METTL14-SMN interaction regulates RNA m 6 A homeostasis

doi: 10.1038/s44319-025-00590-7

Figure Lengend Snippet: ( A ) Sanger sequencing confirmation of Mettl14 arginine methylation deficient mouse model. In total, 13 arginine resides located at the C-terminal disordered region of Mettl14 were mutated to lysine residues. ( B ) The arginine methylation levels of Mettl14 in WT, heterozygous (WT/RK), and homozygous (RK/RK) mice were detected by IP-western blot using tissue lysates from mouse spleen and thymus. ( C ) The protein expression levels of several DNA repair genes, including BRCA1, ATRIP, and PALB2, were detected by western blot using Thymus tissues from WT, WT/RK, and RK/RK mice. ( D ) Mettl14 arginine methylation deficiency increases the population of primitive hematopoietic cells (LK cells). ** P = 0.0019. ( E ) Mettl14 arginine methylation deficiency increases the population of myeloid (Mac1 + Gr1 + ) cells in the BM, but not in the spleen. * P = 0.013. ( F ) Mettl14 arginine methylation deficiency decreases the B lymphoid (B220 + ) population in the BM, but not in the spleen. * P = 0.011. ( G ) Mettl14 arginine methylation deficiency decreases the T lymphoid (CD3 + ) population in the BM, but not in the spleen. Data from three independent replicates were analyzed by Student’s t test and shown as mean ± SD. ** P = 0.0097. .

Article Snippet: Rabbit anti-PALB2 antibody , Proteintech , 14340-1-AP.

Techniques: Sequencing, Methylation, Western Blot, Expressing

Journal: Nucleic Acids Research

Article Title: Profiling BRCA1-BRCT interactions and their functional relevance at amino acid resolution

doi: 10.1093/nar/gkaf848

Figure Lengend Snippet: Identification of novel interaction modules between the BRCT domains and ABRAXAS1 and CtIP. ( A ) Superimposition of Y2H data onto the solved crystal structure of the BRCT domains bound to the ABRAXAS1 peptide (PDB: 4Y18). ( B ) Superimposition of Y2H data onto the solved crystal structure of the BRCT domains bound to the CtIP peptide (PDB: 1Y98). For both panels (A) and (B), the score for each residue was calculated by summing the ENRICH2 scores of the individual amino acid substitutions that negatively affected binding. Darker green colouration indicates residues whose mutation led to more severe disruption of binding. ( C ) IP assay using TY1 antibody in HEK 293T cells overexpressing WT or mutant BRCA1-TY1 to assess its interaction with ABRAXAS1, BRIP1, and CtIP at 3 h post-irradiation with 5 Gy. Tubulin serves as a loading control (EV: empty vector). ( D ) Quantification of RAD51 foci in indicated RPE1 hTERT cells virally complemented with EV, BRCA1 WT, or variants by immunofluorescence (IF) at 3 h post-irradiation with 5 Gy for different BRCA1 variants ( n = 3, representing mean ± SEM). P- value was calculated using ANOVA, followed by multiple comparison Dunnett test comparing the mean values to TP53 KO. Note: TP53 KO is expressing endogenously tagged BRCA1-TY1. ( E ) Clonogenic survival assay in RPE1 hTERT cells comparing the sensitivity of different BRCA1 variants to increasing concentrations of olaparib ( n = 3, representing mean ± SEM). Note: TP53 KO is expressing endogenously tagged BRCA1-TY1. ( F ) IP assay using TY1 antibody in HEK 293T cells overexpressing WT or mutant BRCA1-TY1, showing interactions with BARD1 and PALB2 at 3 h post-irradiation with 5 Gy. Tubulin serves as a loading control (EV: empty vector). Dotted line indicates exclusion of lanes; the compiled lanes originate from the same blot.

Article Snippet: The following primary antibodies were used: TY (Diagenode, C15200054), BRCA1 (Millipore, 07-434), ABRAXAS1 (Abcam, ab139191), BRIP1 (Sigma–Aldrich, B1310-200), CtIP (Millipore, MABE1060), BARD1 (Bethyl, A300-263A), PALB2 (Cell Signaling Technology, #30253), and Tubulin [Sigma–Aldrich, T6199 (Clone DM1A)].

Techniques: Residue, Binding Assay, Mutagenesis, Disruption, Irradiation, Control, Plasmid Preparation, Immunofluorescence, Comparison, Expressing, Clonogenic Cell Survival Assay