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Proteintech usp28
Usp28, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 40 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/usp28/USP28+Antibody/pm41833770-151-3-4
Average 93 stars, based on 40 article reviews

usp28 - by Bioz Stars, 2026-09

93/100 stars

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Transfection:

Article Title: USP28 Promotes Osimertinib Resistance in H1975 NSCLC Cells by Deubiquitinating and Stabilizing SIRT1
Article Snippet: For these assays, a commercially available IP Assay Kit from Beyotime was employed. .. Following the manufacturer guidelines, lysates of untransfected or transfected H1975 and H1975/OSI cells were prepared and added into Protein A magnetic beads previously pre‐incubated with rabbit polyclonal to USP28 (Cat No. 17707–1‐AP, Proteintech), rabbit monoclonal to SIRT1 (Cat No. ab189494, Abcam), or rabbit monoclonal to IgG (Cat No. ab172730, Abcam). ..

Article Title: USP28 Promotes Osimertinib Resistance in H1975 NSCLC Cells by Deubiquitinating and Stabilizing SIRT1.
Article Snippet: For these assays, a commercially available IP Assay Kit from Beyotime was employed. .. Following the manufacturer guidelines, lysates of untransfected or transfected H1975 and H1975/ OSI cells were prepared and added into Protein A magnetic beads previously pre- incubated with rabbit polyclonal to USP28 (Cat No. 17707–1- AP, Proteintech), rabbit monoclonal to SIRT1 (Cat No. ab189494, Abcam), or rabbit monoclonal to IgG (Cat No. ab172730, Abcam). ..

Magnetic Beads:

Incubation:

Article Title: Targeting USP28 inhibits clear cell renal cell carcinoma growth.
Article Snippet: Clear cell renal cell carcinoma (ccRCC), the most common type of kidney cancer, remains challenging to treat due to the lack of effective targeted therapies.. Although cMyc is frequently overexpressed in ccRCC, the mechanisms governing its stability are not well understood.. Here, we identify the deubiquitinating enzyme USP28 as a key regulator of c-Myc protein stability in ccRCC.

Article Title: USP28 Promotes Osimertinib Resistance in H1975 NSCLC Cells by Deubiquitinating and Stabilizing SIRT1
Article Snippet: Protein samples (30 μg per lane) were resolved through SDS‐PAGE and electrophoretically transferred to nitrocellulose membranes (0.45 μm pore size; Beyotime). .. Membranes were incubated overnight at 4°C with the following antibodies: rabbit polyclonal to USP28 (Cat No. 17707–1‐AP, Proteintech, 1 to 12,000), rabbit polyclonal to GLUT1 (Cat No. 21829–1‐AP, Proteintech, 1 to 20,000), rabbit polyclonal to HK2 (Cat No. 22029–1‐AP, Proteintech, 1 to 20,000), rabbit monoclonal to SIRT1 (Cat No. ab189494, Abcam, 1 to 1000), rabbit monoclonal to ubiquitin (Ub, Cat No. ab134953, Abcam, 1 to 5000), or rabbit polyclonal to β‐actin (Cat No. 20536–1‐AP, Proteintech, 1 to 8000). ..

Blocking Assay:

Article Title: FBXW7-mediated CHK2 regulation modulates DNA damage response and cellular stability in Huntington’s disease
Article Snippet: EdU detection was carried out using a Click-iT EdU detection kit according to the manufacturer’s instructions (Invitrogen, Carlsbad, CA, USA). .. After the blocking step, each blot was probed overnight at 4 °C with specific primary antibodies as follows: γH2AX (abcam, Cambridge, MA, USA) HTT (Mab2166, Millipore, Darmstadt, Germany), HTT (1C2, Millipore, Germany), CHK1 (Cell signaling biotechnology, USA), pCHK1 (Cell signaling biotechnology, USA), CHK2 (Cell signaling biotechnology, USA), pCHK2 (Cell signaling biotechnology, USA), p-p53 (abcam, USA), Ku70 (Santa Cruz Biotechnology, USA), FBXW7 (Millipore, Darmstadt, Germany), USP28 (Proteintech, Rosemont, IL, USA), CSN6 (Santa Cruz Biotechnology, USA), and Flag (ThermoFisher, USA). .. Each blot was then incubated with HRP conjugated anti-mouse, or rabbit IgG antibodies (Jackson ImmunoResearch, West Grove, PA, USA) for 1 h at room temperature.

Article Title: FBXW7-mediated CHK2 regulation modulates DNA damage response and cellular stability in Huntington's disease.
Article Snippet: EdU detection was carried out using a Click-iT EdU detection kit according to the manufacturer’s instructions (Invitrogen, Carlsbad, CA, USA). .. After the blocking step, each blot was probed overnight at 4 °C with specific primary antibodies as follows: γH2AX (abcam, Cambridge, MA, USA) HTT (Mab2166, Millipore, Darmstadt, Germany), HTT (1C2, Millipore, Germany), CHK1 (Cell signaling biotechnology, USA), pCHK1 (Cell signaling biotechnology, USA), CHK2 (Cell signaling biotechnology, USA), pCHK2 (Cell signaling biotechnology, USA), p-p53 (abcam, USA), Ku70 (Santa Cruz Biotechnology, USA), FBXW7 (Millipore, Darmstadt, Germany), USP28 (Proteintech, Rosemont, IL, USA), CSN6 (Santa Cruz Biotechnology, USA), and Flag (ThermoFisher, USA). .. Each blot was then incubated with HRP conjugated anti-mouse, or rabbit IgG antibodies (Jackson ImmunoResearch, West Grove, PA, USA) for 1 h at room temperature.

Ubiquitin Proteomics:

Article Title: GMCL1 controls 53BP1 stability and modulates taxane sensitivity
Article Snippet: .. The following antibodies were used: β-actin (1:5000, Sigma-Aldrich A5441), CUL3 (1:1000, Bethyl Laboratories A301-109A), FLAG (1:2000, Sigma-Aldrich F7425), GMCL1 (1:1,000, Proteintech 15575–1-AP), HA (1:2000, Bethyl Laboratories A190-108A), Histone H3 (1:10,000, Abcam, ab1791), p21 (1:1000, Cell Signaling Technology 2947 S), p53 (1:1000, Proteintech 10442–1-AP), pHistone H3 (D2C8) (Ser10, 1:1000, Cell Signaling Technology, #3377), Ubiquitin (p37) (1:1000, Cell Signaling Technology, 58395 S), USP28 (1:1,000, Proteintech 17707–1-AP), 53BP1 (1:2000, Abcam ab36823), α-tubulin (1:5000, Sigma-Aldrich T6074). .. Where indicated, cells were treated with 400 ng/ml Nocodazole (Sigma-Aldrich M1404) for 16 hr, 100 nM paclitaxel for 48 hr, 10 μM MG132 for 3 hr, 2.5 μM MLN4924 for 3 hr, 100 μg/ml cycloheximide (CHX) for the indicated time.

Image Search Results

(A) Schematic of full genome CRISPR screens. After four weeks of growth with no selection pressure, gRNAs selectively lost in WT but not p53 -/- and USP28 -/- cells were used to identify genes whose functions are guarded or masked by EMS. (B) GO Cellular Component Enrichment Analysis on the 79 genes that were considered essential in the WT but neutral or near neutral in p53 -/- and USP28 -/- backgrounds. The RZZ complex was revealed as a top hit, with two of three components, KNTC1 (ROD) and ZWILCH, identified. (C) Growth curve analyses showed that following induction of shRNA-KNTC1, WT (black) cells were fully arrested, while p53 -/- (red), USP28 -/- (green), and 53BP1 -/- (blue) cells continued to grow, albeit at slightly slower rates compared to controls (the respective shRNA clonal line without Dox induction). Data are mean ± SD, N = 3, initial cell count = 100,000, and doxycycline (Dox) at 1 μg/mL. (D) BrdU labeling assays revealed that KNTC1 knockdown has a widespread, detrimental growth impact on WT cells (left) but not p53 -/- , USP28-/-, and 53BP1 -/- cells (center), compared to the non-targeting shRNA control (shRNA-NTC, right). Note that KNTC1 knockdown does have a non-population-level growth impact on EMS-knockout cells ( p53 -/- , USP28 -/- , or 53BP1 -/- ), consistent with (C). Cells were fixed at the end of indicated days, with BrdU (10 μM) added 24 hours prior to fixation. Data are mean ± SD, n > 300, N = 3, statistical significance calculated via T-test with Welch’s correction. (E) Quantification of nuclear p21 intensity at indicated days following knockdown of KNTC1 in WT (left), USP28 -/- (right), or 53BP1 -/- (right) cells. At Day 10 after KNTC1 knockdown, ∼70% of WT cells showed a nuclear p21 intensity that is 3 standard deviations above the mean in control cells, which are defined as high outliers (above dashed blue lines). In contrast, only 10-11% of USP28 -/- or 53BP1 -/- cells were high outliers by Day 10, consistent with the observation that KNTC1 loss has a mild, non-population-level growth impact on EMS-knockout cells. Data are mean signal intensity, n > 240. Black lines indicating median, dashed blue line marking 3 standard deviations above the control mean, and statistical significance calculated via T-test with Welch’s correction.

Journal: bioRxiv

Article Title: Fidelity-Ensuring Consistency of Mitosis is Safeguarded by the 53BP1-USP28-p53 Pathway

doi: 10.64898/2026.03.16.712228

Figure Lengend Snippet: (A) Schematic of full genome CRISPR screens. After four weeks of growth with no selection pressure, gRNAs selectively lost in WT but not p53 -/- and USP28 -/- cells were used to identify genes whose functions are guarded or masked by EMS. (B) GO Cellular Component Enrichment Analysis on the 79 genes that were considered essential in the WT but neutral or near neutral in p53 -/- and USP28 -/- backgrounds. The RZZ complex was revealed as a top hit, with two of three components, KNTC1 (ROD) and ZWILCH, identified. (C) Growth curve analyses showed that following induction of shRNA-KNTC1, WT (black) cells were fully arrested, while p53 -/- (red), USP28 -/- (green), and 53BP1 -/- (blue) cells continued to grow, albeit at slightly slower rates compared to controls (the respective shRNA clonal line without Dox induction). Data are mean ± SD, N = 3, initial cell count = 100,000, and doxycycline (Dox) at 1 μg/mL. (D) BrdU labeling assays revealed that KNTC1 knockdown has a widespread, detrimental growth impact on WT cells (left) but not p53 -/- , USP28-/-, and 53BP1 -/- cells (center), compared to the non-targeting shRNA control (shRNA-NTC, right). Note that KNTC1 knockdown does have a non-population-level growth impact on EMS-knockout cells ( p53 -/- , USP28 -/- , or 53BP1 -/- ), consistent with (C). Cells were fixed at the end of indicated days, with BrdU (10 μM) added 24 hours prior to fixation. Data are mean ± SD, n > 300, N = 3, statistical significance calculated via T-test with Welch’s correction. (E) Quantification of nuclear p21 intensity at indicated days following knockdown of KNTC1 in WT (left), USP28 -/- (right), or 53BP1 -/- (right) cells. At Day 10 after KNTC1 knockdown, ∼70% of WT cells showed a nuclear p21 intensity that is 3 standard deviations above the mean in control cells, which are defined as high outliers (above dashed blue lines). In contrast, only 10-11% of USP28 -/- or 53BP1 -/- cells were high outliers by Day 10, consistent with the observation that KNTC1 loss has a mild, non-population-level growth impact on EMS-knockout cells. Data are mean signal intensity, n > 240. Black lines indicating median, dashed blue line marking 3 standard deviations above the control mean, and statistical significance calculated via T-test with Welch’s correction.

Article Snippet: The following two pairs of primary antibodies for 53BP1, USP28, and p53 and their concentrations were used for PLA: (i) rabbit p53 (Cell Signaling, 9282S, 1:400) and mouse 53BP1 (Sigma, MAB3802, 1:400), and (ii) rabbit USP28 (Thermo Fisher, PA5-52346, 1:200) and mouse p53 (Santa Cruz, sc-126, 1:400).

Techniques: CRISPR, Selection, shRNA, Cell Characterization, Labeling, Knockdown, Control, Knock-Out

(A) Quantification of γH2AX foci per cell in USP28 -/- G1 cells showed no increase following loss of KNTC1. n > 60, N =2, no statistical difference was found between the two experiments (not shown). Graphs showed combined data, with statistical significance calculated via T-test with Welch’s correction. (B) Quantification of γH2AX foci per cell in USP28 -/- cells in S/G2 showed no significant increase following loss of KNTC1 between control and Day 6, or between Day 6 and Day 10. However, a small but significant difference is seen when comparing control to Day 10. Closer examination showed minimal difference in mean number of foci, but the presence of a small number of cells (∼3% at both Day 6 and Day 10) with significantly higher foci counts. n > 60, N =2, no statistical difference was found between the two experiments (not shown), and graphs showed combined data. Black line at median, blue line at 3 standard deviations above the mean (to control cells), and statistical significance calculated via T-test with Welch’s correction. (C) Representative images of γH2AX foci in USP28 -/- control cells (no induction) and at Day 10 following shRNA-KNTC1 induction. Top panels showed G1 cells, identified by the absence of SAS-6 at centrosomes (marked by centrin); bottom panels showed S/G2, identified by the presence of SAS-6 at centrosomes.

Journal: bioRxiv

Article Title: Fidelity-Ensuring Consistency of Mitosis is Safeguarded by the 53BP1-USP28-p53 Pathway

doi: 10.64898/2026.03.16.712228

Figure Lengend Snippet: (A) Quantification of γH2AX foci per cell in USP28 -/- G1 cells showed no increase following loss of KNTC1. n > 60, N =2, no statistical difference was found between the two experiments (not shown). Graphs showed combined data, with statistical significance calculated via T-test with Welch’s correction. (B) Quantification of γH2AX foci per cell in USP28 -/- cells in S/G2 showed no significant increase following loss of KNTC1 between control and Day 6, or between Day 6 and Day 10. However, a small but significant difference is seen when comparing control to Day 10. Closer examination showed minimal difference in mean number of foci, but the presence of a small number of cells (∼3% at both Day 6 and Day 10) with significantly higher foci counts. n > 60, N =2, no statistical difference was found between the two experiments (not shown), and graphs showed combined data. Black line at median, blue line at 3 standard deviations above the mean (to control cells), and statistical significance calculated via T-test with Welch’s correction. (C) Representative images of γH2AX foci in USP28 -/- control cells (no induction) and at Day 10 following shRNA-KNTC1 induction. Top panels showed G1 cells, identified by the absence of SAS-6 at centrosomes (marked by centrin); bottom panels showed S/G2, identified by the presence of SAS-6 at centrosomes.

Techniques: Control, shRNA

(A) Analyses of clonal isolations for cells undergoing CRISPR-mediated KNTC1 targeting in p53 -/- , USP28 -/- , 53BP1 -/- , and WT backgrounds. The table starts with the total number of clones examined, among which how many were visibly arrested. Also tabulated are numbers of clones checked for KNTC1 staining at early mitotic kinetochores, of which how many exhibited normal or disrupted (reduced or absent) signals. Indicated numbers of clones with disrupted signals were further selected for sequencing, determining if they are heterozygous or homozygous KNTC1 knockouts. (B) Representative images of normal, reduced, and absent KNTC1 signals in p53 -/- ; KNTC1 +/+ (WT), p53 -/- ; KNTC1 +/- (heterozygous knockout), and p53 -/- ; KNTC1 -/- (homozygous knockout), respectively. (C) Quantification of mitotic durations prior to slippage in the presence of nocodazole. KNTC1 +/+ cells in both p53 -/- and WT backgrounds could arrest in nocodazole-treated mitosis for a mean duration of 11.5 and 10.7 hours, respectively, before slippage. In contrast, both KNTC1 +/- (heterozygous) and KNTC1 -/- (homozygous) cells in the p53 -/- background exited mitosis after a short arrest of 1.8 hours, indicating a severe disruption of SAC. The singular KNTC1 +/- clone (Singleton-Het) survived in the WT background, however, could stay in mitotic arrest for a mean of 8.3 hours, indicating a mildly compromised SAC. n > 200, nocodazole added at 50 ng/mL. (D) Quantification of normal mitotic duration in the absence of nocodazole perturbation. KNTC1 +/- and KNTC1 -/- cells obtained from the p53 -/- background showed a small increase in average mitotic duration from 23 to 34 and 36 minutes, respectively, suggesting the presence of sub-optimal kinetochore function. The singular heterozygous KNTC1 clone survived in the WT background in our screen showed no significant increase in mitotic duration, remaining at 24 minutes, suggesting the presence of functional kinetochores or SAC. n > 200, statistical significance calculated via T-test with Welch’s correction.

Journal: bioRxiv

Article Title: Fidelity-Ensuring Consistency of Mitosis is Safeguarded by the 53BP1-USP28-p53 Pathway

doi: 10.64898/2026.03.16.712228

Figure Lengend Snippet: (A) Analyses of clonal isolations for cells undergoing CRISPR-mediated KNTC1 targeting in p53 -/- , USP28 -/- , 53BP1 -/- , and WT backgrounds. The table starts with the total number of clones examined, among which how many were visibly arrested. Also tabulated are numbers of clones checked for KNTC1 staining at early mitotic kinetochores, of which how many exhibited normal or disrupted (reduced or absent) signals. Indicated numbers of clones with disrupted signals were further selected for sequencing, determining if they are heterozygous or homozygous KNTC1 knockouts. (B) Representative images of normal, reduced, and absent KNTC1 signals in p53 -/- ; KNTC1 +/+ (WT), p53 -/- ; KNTC1 +/- (heterozygous knockout), and p53 -/- ; KNTC1 -/- (homozygous knockout), respectively. (C) Quantification of mitotic durations prior to slippage in the presence of nocodazole. KNTC1 +/+ cells in both p53 -/- and WT backgrounds could arrest in nocodazole-treated mitosis for a mean duration of 11.5 and 10.7 hours, respectively, before slippage. In contrast, both KNTC1 +/- (heterozygous) and KNTC1 -/- (homozygous) cells in the p53 -/- background exited mitosis after a short arrest of 1.8 hours, indicating a severe disruption of SAC. The singular KNTC1 +/- clone (Singleton-Het) survived in the WT background, however, could stay in mitotic arrest for a mean of 8.3 hours, indicating a mildly compromised SAC. n > 200, nocodazole added at 50 ng/mL. (D) Quantification of normal mitotic duration in the absence of nocodazole perturbation. KNTC1 +/- and KNTC1 -/- cells obtained from the p53 -/- background showed a small increase in average mitotic duration from 23 to 34 and 36 minutes, respectively, suggesting the presence of sub-optimal kinetochore function. The singular heterozygous KNTC1 clone survived in the WT background in our screen showed no significant increase in mitotic duration, remaining at 24 minutes, suggesting the presence of functional kinetochores or SAC. n > 200, statistical significance calculated via T-test with Welch’s correction.

Techniques: CRISPR, Clone Assay, Staining, Sequencing, Knock-Out, Disruption, Functional Assay

Representative images of normal (KNTC1 +/+ ), reduced ( KNTC1 +/- ), and absent ( KNTC1 -/- ) KNTC1signal in the USP28 -/- , 53BP1 -/- , or WT background as indicated. KNTC1 genotypes were confirmed by sequencing. No KNTC1 -/- clones could be isolated from the WT background.

Journal: bioRxiv

Article Title: Fidelity-Ensuring Consistency of Mitosis is Safeguarded by the 53BP1-USP28-p53 Pathway

doi: 10.64898/2026.03.16.712228

Figure Lengend Snippet: Representative images of normal (KNTC1 +/+ ), reduced ( KNTC1 +/- ), and absent ( KNTC1 -/- ) KNTC1signal in the USP28 -/- , 53BP1 -/- , or WT background as indicated. KNTC1 genotypes were confirmed by sequencing. No KNTC1 -/- clones could be isolated from the WT background.

Techniques: Sequencing, Clone Assay, Isolation

(A & B) Cells arrested at G2 by RO3306 (9.5 μM) were released into mitosis under the indicated conditions for the indicated amounts of time before fixation for PLA analysis of complex formation. In control cells no increase in the total area ( A ) or number ( B ) of PLA foci was seen up to 40 minutes after RO3306 washout (first panel). In the presence of nocodazole (50 ng/mL), an increase in both the area and number of foci was seen between 40 and 80 minutes after washout (second panel) but not before. Following inducible KNTC1 knockdown (Day 3 under doxycycline), an increase in both the area and number of PLA foci was detectable between 10 and 20 minutes after washout, with an additional significant increase between 20 and 30 minutes (third panel). PLA reactions were carried out using primary antibodies against endogenous 53BP1 and p53, n > 75, area quantified as the number of pixels above the background threshold, and statistical significances calculated via T-tests with Welch’s correction. Similar PLA results were seen with antibodies against 53BP1 and USP28 (data not shown; see methods). (C) Mitotic durations of WT cells treated with low-dose ProTAME (2 μM) resembled those of KNTC1-knockdown cells (left) but did not induce fast formation of 53BP1-USP28-p53 complexes in early mitosis (middle and right). The mean duration in both conditions is ∼36 minutes with no significant difference in distributions (calculated by T-test with Welch’s correction). Cells arrested at G2 with RO3306 (9.5 μM) were released into mitosis in the presence of ProTAME (2 μM) for the indicated amounts of time, fixed, and examined by PLA with primary antibodies against endogenous 53BP1 and p53. No increase in total area (middle) or number (right) of PLA foci was seen up to 40 minutes after RO3306 washout. n > 75, statistical significances calculated via T-tests with Welch’s correction.

Journal: bioRxiv

Article Title: Fidelity-Ensuring Consistency of Mitosis is Safeguarded by the 53BP1-USP28-p53 Pathway

doi: 10.64898/2026.03.16.712228

Figure Lengend Snippet: (A & B) Cells arrested at G2 by RO3306 (9.5 μM) were released into mitosis under the indicated conditions for the indicated amounts of time before fixation for PLA analysis of complex formation. In control cells no increase in the total area ( A ) or number ( B ) of PLA foci was seen up to 40 minutes after RO3306 washout (first panel). In the presence of nocodazole (50 ng/mL), an increase in both the area and number of foci was seen between 40 and 80 minutes after washout (second panel) but not before. Following inducible KNTC1 knockdown (Day 3 under doxycycline), an increase in both the area and number of PLA foci was detectable between 10 and 20 minutes after washout, with an additional significant increase between 20 and 30 minutes (third panel). PLA reactions were carried out using primary antibodies against endogenous 53BP1 and p53, n > 75, area quantified as the number of pixels above the background threshold, and statistical significances calculated via T-tests with Welch’s correction. Similar PLA results were seen with antibodies against 53BP1 and USP28 (data not shown; see methods). (C) Mitotic durations of WT cells treated with low-dose ProTAME (2 μM) resembled those of KNTC1-knockdown cells (left) but did not induce fast formation of 53BP1-USP28-p53 complexes in early mitosis (middle and right). The mean duration in both conditions is ∼36 minutes with no significant difference in distributions (calculated by T-test with Welch’s correction). Cells arrested at G2 with RO3306 (9.5 μM) were released into mitosis in the presence of ProTAME (2 μM) for the indicated amounts of time, fixed, and examined by PLA with primary antibodies against endogenous 53BP1 and p53. No increase in total area (middle) or number (right) of PLA foci was seen up to 40 minutes after RO3306 washout. n > 75, statistical significances calculated via T-tests with Welch’s correction.

Techniques: Control, Knockdown

Representative images of PLA foci using primary antibodies against endogenous p53 and 53BP1 to visualize 53BP1-USP28-p53 complexes in mitosis. Cells were arrested at G2 by RO3306 and released into mitosis under indicated conditions for indicated amounts of time before being fixed and examined by PLA. Cells were released into mitosis without additional drugs (control), in the presence of nocodazole (NOC, 50 ng/mL) or ProTAME (2 μM), or following KNTC1-knockdown (doxycycline 1 μg/mL, Day 3) as indicated.

Journal: bioRxiv

Article Title: Fidelity-Ensuring Consistency of Mitosis is Safeguarded by the 53BP1-USP28-p53 Pathway

doi: 10.64898/2026.03.16.712228

Figure Lengend Snippet: Representative images of PLA foci using primary antibodies against endogenous p53 and 53BP1 to visualize 53BP1-USP28-p53 complexes in mitosis. Cells were arrested at G2 by RO3306 and released into mitosis under indicated conditions for indicated amounts of time before being fixed and examined by PLA. Cells were released into mitosis without additional drugs (control), in the presence of nocodazole (NOC, 50 ng/mL) or ProTAME (2 μM), or following KNTC1-knockdown (doxycycline 1 μg/mL, Day 3) as indicated.

Techniques: Control, Knockdown

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usp28 (Proteintech)

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