dok 2 Search Results


dok 2  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology dok 2
Dok 2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/dok+2/Dok-2+Antibody/pmc02213020-74-15-17
Average 93 stars, based on 1 article reviews
dok 2 - by Bioz Stars, 2026-09
93/100 stars
  Buy from Supplier
rabbit anti akt  (Proteintech)
92
Proteintech rabbit anti akt
Rabbit Anti Akt, supplied by Proteintech, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/dok+2/DOK2+Antibody/10__1155_slash_2024_slash_4822900-51-164-167
Average 92 stars, based on 1 article reviews
rabbit anti akt - by Bioz Stars, 2026-09
92/100 stars
  Buy from Supplier
copy number variation dok2 hs00497516 cn  (Thermo Fisher)
90
Thermo Fisher copy number variation dok2 hs00497516 cn
(A) Depicts copy number alterations in WM patients progressing on ibrutinib. Each square represents a chromosome. Losses are coloured in blue, gains in red, and green corresponds to normal copy number. Deletion of chromosome 6q was present in 100% patients at baseline and progression, including homozygous loss in 33% cases at baseline and in 60% at the time of ibrutinib progression. In IBR3 the homozygous deletion was inferred to be subclonal, affecting to a third of the tumour population at baseline and increasing at progression. Del8p was observed in 2/3 cases (66%) at baseline and in 4/5 cases (80%) at progression, and includes BLK, and <t>DOK2.</t> The patient without del8p (IBR1) harboured a truncating mutation in DOK2. Finally, 3q amplification was absent at baseline, but present in 40% patients at the time of progression. (B) Depicts genomic alterations in WM patients progressing on ibrutinib. Patients (represented with lines) are displayed by time to progression (TTP). For IBR1, IBR2 and IBR3, the proportion of persistent mutations (horizontal bars) is shown with respect to the mutations present at only one of the time points (vertical bars). On the right, the most remarkable alterations are shown for each patient: first, recurrent copy number variations and then, somatic mutations. Patients with mutated BTKCys481 also harboured other mutations which affect the B-cell receptor pathway. Other recurrently mutated genes were also identified (i.e. ITCH, RNF19B and TOLLIP), as well as copy number alterations, such as 3q amplification with loss of heterozygosity, with an embedded uniparental disomy that included TBL1XR1 in the two patients lacking BTK mutations.
Copy Number Variation Dok2 Hs00497516 Cn, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/dok+2/Copy+Number+Variation+DOK2%2C+Hs00497516_cn/pmc07299825-80-21-41
Average 90 stars, based on 1 article reviews
copy number variation dok2 hs00497516 cn - by Bioz Stars, 2026-09
90/100 stars
  Buy from Supplier
ki 67 antibody  (Bioss)
92
Bioss ki 67 antibody
(A) Depicts copy number alterations in WM patients progressing on ibrutinib. Each square represents a chromosome. Losses are coloured in blue, gains in red, and green corresponds to normal copy number. Deletion of chromosome 6q was present in 100% patients at baseline and progression, including homozygous loss in 33% cases at baseline and in 60% at the time of ibrutinib progression. In IBR3 the homozygous deletion was inferred to be subclonal, affecting to a third of the tumour population at baseline and increasing at progression. Del8p was observed in 2/3 cases (66%) at baseline and in 4/5 cases (80%) at progression, and includes BLK, and <t>DOK2.</t> The patient without del8p (IBR1) harboured a truncating mutation in DOK2. Finally, 3q amplification was absent at baseline, but present in 40% patients at the time of progression. (B) Depicts genomic alterations in WM patients progressing on ibrutinib. Patients (represented with lines) are displayed by time to progression (TTP). For IBR1, IBR2 and IBR3, the proportion of persistent mutations (horizontal bars) is shown with respect to the mutations present at only one of the time points (vertical bars). On the right, the most remarkable alterations are shown for each patient: first, recurrent copy number variations and then, somatic mutations. Patients with mutated BTKCys481 also harboured other mutations which affect the B-cell receptor pathway. Other recurrently mutated genes were also identified (i.e. ITCH, RNF19B and TOLLIP), as well as copy number alterations, such as 3q amplification with loss of heterozygosity, with an embedded uniparental disomy that included TBL1XR1 in the two patients lacking BTK mutations.
Ki 67 Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/dok+2/DOK2+(Tyr139)+Polyclonal+Antibody/pm34153644-116-15-19
Average 92 stars, based on 1 article reviews
ki 67 antibody - by Bioz Stars, 2026-09
92/100 stars
  Buy from Supplier
anti-ras, dok1, dok2, ras-gtpase activating protein (rasgap) mab  (Becton Dickinson)
90
Becton Dickinson anti-ras, dok1, dok2, ras-gtpase activating protein (rasgap) mab
(A) Depicts copy number alterations in WM patients progressing on ibrutinib. Each square represents a chromosome. Losses are coloured in blue, gains in red, and green corresponds to normal copy number. Deletion of chromosome 6q was present in 100% patients at baseline and progression, including homozygous loss in 33% cases at baseline and in 60% at the time of ibrutinib progression. In IBR3 the homozygous deletion was inferred to be subclonal, affecting to a third of the tumour population at baseline and increasing at progression. Del8p was observed in 2/3 cases (66%) at baseline and in 4/5 cases (80%) at progression, and includes BLK, and <t>DOK2.</t> The patient without del8p (IBR1) harboured a truncating mutation in DOK2. Finally, 3q amplification was absent at baseline, but present in 40% patients at the time of progression. (B) Depicts genomic alterations in WM patients progressing on ibrutinib. Patients (represented with lines) are displayed by time to progression (TTP). For IBR1, IBR2 and IBR3, the proportion of persistent mutations (horizontal bars) is shown with respect to the mutations present at only one of the time points (vertical bars). On the right, the most remarkable alterations are shown for each patient: first, recurrent copy number variations and then, somatic mutations. Patients with mutated BTKCys481 also harboured other mutations which affect the B-cell receptor pathway. Other recurrently mutated genes were also identified (i.e. ITCH, RNF19B and TOLLIP), as well as copy number alterations, such as 3q amplification with loss of heterozygosity, with an embedded uniparental disomy that included TBL1XR1 in the two patients lacking BTK mutations.
Anti Ras, Dok1, Dok2, Ras Gtpase Activating Protein (Rasgap) Mab, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/dok+2/dok2+ab/pm16330532-26-0-12
Average 90 stars, based on 1 article reviews
anti-ras, dok1, dok2, ras-gtpase activating protein (rasgap) mab - by Bioz Stars, 2026-09
90/100 stars
  Buy from Supplier
gene exp dok2 hs00182758 m1  (Thermo Fisher)
86
Thermo Fisher gene exp dok2 hs00182758 m1
(A) Depicts copy number alterations in WM patients progressing on ibrutinib. Each square represents a chromosome. Losses are coloured in blue, gains in red, and green corresponds to normal copy number. Deletion of chromosome 6q was present in 100% patients at baseline and progression, including homozygous loss in 33% cases at baseline and in 60% at the time of ibrutinib progression. In IBR3 the homozygous deletion was inferred to be subclonal, affecting to a third of the tumour population at baseline and increasing at progression. Del8p was observed in 2/3 cases (66%) at baseline and in 4/5 cases (80%) at progression, and includes BLK, and <t>DOK2.</t> The patient without del8p (IBR1) harboured a truncating mutation in DOK2. Finally, 3q amplification was absent at baseline, but present in 40% patients at the time of progression. (B) Depicts genomic alterations in WM patients progressing on ibrutinib. Patients (represented with lines) are displayed by time to progression (TTP). For IBR1, IBR2 and IBR3, the proportion of persistent mutations (horizontal bars) is shown with respect to the mutations present at only one of the time points (vertical bars). On the right, the most remarkable alterations are shown for each patient: first, recurrent copy number variations and then, somatic mutations. Patients with mutated BTKCys481 also harboured other mutations which affect the B-cell receptor pathway. Other recurrently mutated genes were also identified (i.e. ITCH, RNF19B and TOLLIP), as well as copy number alterations, such as 3q amplification with loss of heterozygosity, with an embedded uniparental disomy that included TBL1XR1 in the two patients lacking BTK mutations.
Gene Exp Dok2 Hs00182758 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/dok+2/Gene+Exp%2E+DOK2%2C+Hs00182758_m1/pm21266183-70-21--1
Average 86 stars, based on 1 article reviews
gene exp dok2 hs00182758 m1 - by Bioz Stars, 2026-09
86/100 stars
  Buy from Supplier
dok-2 / (dok-2 ko) mice  (Japan SLC inc)
90
Japan SLC inc dok-2 / (dok-2 ko) mice
(A) Depicts copy number alterations in WM patients progressing on ibrutinib. Each square represents a chromosome. Losses are coloured in blue, gains in red, and green corresponds to normal copy number. Deletion of chromosome 6q was present in 100% patients at baseline and progression, including homozygous loss in 33% cases at baseline and in 60% at the time of ibrutinib progression. In IBR3 the homozygous deletion was inferred to be subclonal, affecting to a third of the tumour population at baseline and increasing at progression. Del8p was observed in 2/3 cases (66%) at baseline and in 4/5 cases (80%) at progression, and includes BLK, and <t>DOK2.</t> The patient without del8p (IBR1) harboured a truncating mutation in DOK2. Finally, 3q amplification was absent at baseline, but present in 40% patients at the time of progression. (B) Depicts genomic alterations in WM patients progressing on ibrutinib. Patients (represented with lines) are displayed by time to progression (TTP). For IBR1, IBR2 and IBR3, the proportion of persistent mutations (horizontal bars) is shown with respect to the mutations present at only one of the time points (vertical bars). On the right, the most remarkable alterations are shown for each patient: first, recurrent copy number variations and then, somatic mutations. Patients with mutated BTKCys481 also harboured other mutations which affect the B-cell receptor pathway. Other recurrently mutated genes were also identified (i.e. ITCH, RNF19B and TOLLIP), as well as copy number alterations, such as 3q amplification with loss of heterozygosity, with an embedded uniparental disomy that included TBL1XR1 in the two patients lacking BTK mutations.
Dok 2 / (Dok 2 Ko) Mice, supplied by Japan SLC inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/dok+2/dok+2++++dok+2+ko++mice/pm27450811-38-22-5
Average 90 stars, based on 1 article reviews
dok-2 / (dok-2 ko) mice - by Bioz Stars, 2026-09
90/100 stars
  Buy from Supplier
anti-dok1 (tyr-362) [dok2 (tyr-337)], phosphospecific antibody  (Antibodies Inc)
98
Antibodies Inc anti-dok1 (tyr-362) [dok2 (tyr-337)], phosphospecific antibody
(A) Depicts copy number alterations in WM patients progressing on ibrutinib. Each square represents a chromosome. Losses are coloured in blue, gains in red, and green corresponds to normal copy number. Deletion of chromosome 6q was present in 100% patients at baseline and progression, including homozygous loss in 33% cases at baseline and in 60% at the time of ibrutinib progression. In IBR3 the homozygous deletion was inferred to be subclonal, affecting to a third of the tumour population at baseline and increasing at progression. Del8p was observed in 2/3 cases (66%) at baseline and in 4/5 cases (80%) at progression, and includes BLK, and <t>DOK2.</t> The patient without del8p (IBR1) harboured a truncating mutation in DOK2. Finally, 3q amplification was absent at baseline, but present in 40% patients at the time of progression. (B) Depicts genomic alterations in WM patients progressing on ibrutinib. Patients (represented with lines) are displayed by time to progression (TTP). For IBR1, IBR2 and IBR3, the proportion of persistent mutations (horizontal bars) is shown with respect to the mutations present at only one of the time points (vertical bars). On the right, the most remarkable alterations are shown for each patient: first, recurrent copy number variations and then, somatic mutations. Patients with mutated BTKCys481 also harboured other mutations which affect the B-cell receptor pathway. Other recurrently mutated genes were also identified (i.e. ITCH, RNF19B and TOLLIP), as well as copy number alterations, such as 3q amplification with loss of heterozygosity, with an embedded uniparental disomy that included TBL1XR1 in the two patients lacking BTK mutations.
Anti Dok1 (Tyr 362) [Dok2 (Tyr 337)], Phosphospecific Antibody, supplied by Antibodies Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/dok+2/Anti-Dok1+(Tyr-362)+%5BDok2+(Tyr-337)%5D%2C+Phosphospecific+Antibody/antibodies+inc___dp2241
Average 98 stars, based on 1 article reviews
anti-dok1 (tyr-362) [dok2 (tyr-337)], phosphospecific antibody - by Bioz Stars, 2026-09
98/100 stars
  Buy from Supplier
dok2 nm 010071 mouse tagged orf clone  (OriGene)
N/A
Dok2 Myc DDK tagged Mouse docking protein 2 Dok2
   Buy from Supplier
dok2 nm 003974 human mass spec standard  (OriGene)
N/A
DOK2 MS Standard C13 and N15 labeled recombinant protein NP 003965
   Buy from Supplier
dok2 rat shrna plasmid  (OriGene)
N/A
Dok2 Rat 4 unique 29mer shRNA constructs in retroviral untagged vector
   Buy from Supplier
dok2 nm 001106048 rat tagged orf clone  (OriGene)
N/A
Dok2 Myc DDK tagged ORF Rat docking protein 2 Dok2 10 ug
   Buy from Supplier

Image Search Results


(A) Depicts copy number alterations in WM patients progressing on ibrutinib. Each square represents a chromosome. Losses are coloured in blue, gains in red, and green corresponds to normal copy number. Deletion of chromosome 6q was present in 100% patients at baseline and progression, including homozygous loss in 33% cases at baseline and in 60% at the time of ibrutinib progression. In IBR3 the homozygous deletion was inferred to be subclonal, affecting to a third of the tumour population at baseline and increasing at progression. Del8p was observed in 2/3 cases (66%) at baseline and in 4/5 cases (80%) at progression, and includes BLK, and DOK2. The patient without del8p (IBR1) harboured a truncating mutation in DOK2. Finally, 3q amplification was absent at baseline, but present in 40% patients at the time of progression. (B) Depicts genomic alterations in WM patients progressing on ibrutinib. Patients (represented with lines) are displayed by time to progression (TTP). For IBR1, IBR2 and IBR3, the proportion of persistent mutations (horizontal bars) is shown with respect to the mutations present at only one of the time points (vertical bars). On the right, the most remarkable alterations are shown for each patient: first, recurrent copy number variations and then, somatic mutations. Patients with mutated BTKCys481 also harboured other mutations which affect the B-cell receptor pathway. Other recurrently mutated genes were also identified (i.e. ITCH, RNF19B and TOLLIP), as well as copy number alterations, such as 3q amplification with loss of heterozygosity, with an embedded uniparental disomy that included TBL1XR1 in the two patients lacking BTK mutations.

Journal: British journal of haematology

Article Title: Genomic Evolution of Ibrutinib Resistant Clones in Waldenström Macroglobulinemia

doi: 10.1111/bjh.16463

Figure Lengend Snippet: (A) Depicts copy number alterations in WM patients progressing on ibrutinib. Each square represents a chromosome. Losses are coloured in blue, gains in red, and green corresponds to normal copy number. Deletion of chromosome 6q was present in 100% patients at baseline and progression, including homozygous loss in 33% cases at baseline and in 60% at the time of ibrutinib progression. In IBR3 the homozygous deletion was inferred to be subclonal, affecting to a third of the tumour population at baseline and increasing at progression. Del8p was observed in 2/3 cases (66%) at baseline and in 4/5 cases (80%) at progression, and includes BLK, and DOK2. The patient without del8p (IBR1) harboured a truncating mutation in DOK2. Finally, 3q amplification was absent at baseline, but present in 40% patients at the time of progression. (B) Depicts genomic alterations in WM patients progressing on ibrutinib. Patients (represented with lines) are displayed by time to progression (TTP). For IBR1, IBR2 and IBR3, the proportion of persistent mutations (horizontal bars) is shown with respect to the mutations present at only one of the time points (vertical bars). On the right, the most remarkable alterations are shown for each patient: first, recurrent copy number variations and then, somatic mutations. Patients with mutated BTKCys481 also harboured other mutations which affect the B-cell receptor pathway. Other recurrently mutated genes were also identified (i.e. ITCH, RNF19B and TOLLIP), as well as copy number alterations, such as 3q amplification with loss of heterozygosity, with an embedded uniparental disomy that included TBL1XR1 in the two patients lacking BTK mutations.

Article Snippet: Validation of CNA in chromosome 8p was performed in tumour and germline samples with the TaqMan RT-PCR assays for copy number: Hs00497516_cn ( DOK2 ) and Hs00132843_cn ( TNFRSF10B ), and expression: Hs00929587_m1 ( DOK2 ) and Hs00366278_m1 ( TNFRSF10B ) (Thermo Fisher Scientific, Waltham MA).

Techniques: Mutagenesis, Amplification